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1. Brito LP, Lerário AM, Bronstein MD, Soares IC, Mendonca BB, Fragoso MC: Influence of the fibroblast growth factor receptor 4 expression and the G388R functional polymorphism on Cushing's disease outcome. J Clin Endocrinol Metab; 2010 Oct;95(10):E271-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Influence of the fibroblast growth factor receptor 4 expression and the G388R functional polymorphism on Cushing's disease outcome.
  • CONTEXT: Abnormal FGFR4 expression has been detected in pituitary tumors, especially in larger and invasive adenomas.
  • Then, we hypothesized that FGFR4 expression and genotype could be markers of adverse outcome of Cushing's disease after transsphenoidal surgery.
  • OBJECTIVES: The objective was to investigate whether there is an association between the postoperative outcome of Cushing's disease (remission/recurrence) and the FGFR4 G388R genotype or the FGFR4 expression in corticotrophinomas.
  • FGFR4 expression was assessed by real-time PCR in 18 corticotrophinomas.
  • MAIN OUTCOME MEASURES: The outcome measures included the FGFR4 G388R genotype and FGFR4 expression in postoperative remission and recurrence of Cushing's disease.
  • RESULTS: Homozygosis for FGFR4 glycine (Gly(388)) allele was associated with reduced disease-free survival, in the univariate analysis (hazard ratio of 6.91; 95% confidence interval of 1.14-11.26; P = 0.028).
  • Male gender (P = 0.036), lack of pathology confirmation (P = 0.009), and cortisol levels more than 2 μg/dl in the early postoperative period (P < 0.001) were also significant predictors of Cushing's disease recurrence in the univariate analysis.
  • FGFR4 overexpression was found in 44% of the corticotrophinomas, and it was associated with lower postoperative remission rate (P = 0.009).
  • CONCLUSIONS: Our data suggest that homozygosis for FGFR4 Gly(388) allele and FGFR4 overexpression are associated with higher frequency of postoperative recurrence and persistence of Cushing's disease, respectively.
  • [MeSH-major] Pituitary ACTH Hypersecretion / genetics. Polymorphism, Single Nucleotide. Receptor, Fibroblast Growth Factor, Type 4 / genetics
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / diagnosis. ACTH-Secreting Pituitary Adenoma / genetics. ACTH-Secreting Pituitary Adenoma / surgery. Adolescent. Adult. Amino Acid Substitution / genetics. Arginine / genetics. Child. Female. Gene Expression / physiology. Glycine / genetics. Humans. Hypophysectomy. Male. Middle Aged. Pituitary Neoplasms / diagnosis. Pituitary Neoplasms / genetics. Pituitary Neoplasms / surgery. Prognosis. Recurrence. Retrospective Studies. Treatment Outcome. Young Adult

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  • (PMID = 20660043.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 94ZLA3W45F / Arginine; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 4; TE7660XO1C / Glycine
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2. Pecori Giraldi F, Scaroni C, Arvat E, Martin M, Giordano R, Albiger N, Leao AA, Picu A, Mantero F, Cavagnini F: Effect of protracted treatment with rosiglitazone, a PPARgamma agonist, in patients with Cushing's disease. Clin Endocrinol (Oxf); 2006 Feb;64(2):219-24
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of protracted treatment with rosiglitazone, a PPARgamma agonist, in patients with Cushing's disease.
  • OBJECTIVE: Cushing's disease, hypercortisolism due to a pituitary ACTH-secreting tumour, is a highly morbid illness as yet without effective medical therapy.
  • Recent studies have demonstrated that peroxisome proliferator-activated receptor gamma (PPARgamma) agonists effectively suppress ACTH secretion in a murine tumoral corticotroph cell line, but the few studies conducted so far in patients with ACTH-secreting pituitary adenomas have yielded variable results.
  • DESIGN: Ten patients with Cushing's disease were treated with 4-16 mg rosiglitazone p.o. daily for 1-8 months (median 3 months) and plasma ACTH and cortisol, urinary free cortisol (UFC), as well as parameters of insulin sensitivity, were recorded.
  • RESULTS: The acute challenge with rosiglitazone did not significantly modify plasma ACTH and cortisol levels.
  • In the others, UFC as well as plasma ACTH and cortisol decrements were inscribed within wide, random oscillations indicating that disease activity was substantially unchanged.
  • Insulin sensitivity was ameliorated in most patients, without relation to ACTH or cortisol secretion.
  • CONCLUSIONS: Although effective in a subset of patients, protracted rosiglitazone administration did not consistently restrain ACTH and cortisol secretion in patients with Cushing's disease.
  • Further investigations are needed to fully define the therapeutic potential of PPARgamma agonists in this disorder.
  • [MeSH-major] Peroxisome Proliferator-Activated Receptors / agonists. Pituitary ACTH Hypersecretion / drug therapy. Thiazolidinediones / administration & dosage

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  • (PMID = 16430724.001).
  • [ISSN] 0300-0664
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Peroxisome Proliferator-Activated Receptors; 0 / Thiazolidinediones; 05V02F2KDG / rosiglitazone; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
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3. Johnson MD, Fan X, Bourne P, Walters D: Neuronal differentiation and expression of neural epitopes in pituitary adenomas. J Histochem Cytochem; 2007 Dec;55(12):1265-71
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  • [Title] Neuronal differentiation and expression of neural epitopes in pituitary adenomas.
  • Neural transdifferentiation is increasingly recognized in neural crest and neural stem cell tumors.
  • Neuronal differentiation has been anecdotally described primarily in somatotroph cell adenomas associated with acromegaly, but its prevalence in adenomas and relationship to adenoma type has not been completely established.
  • In this study we performed a retrospective morphological and immunohistochemical analysis of neurofilament, phosphoneurofilament, Neu-N, class III tubulin, and Hu in WHO grade I pituitary adenomas.
  • Limited numbers of cells with neuronal features and neuron-associated epitopes may be more common in pituitary adenomas than previously recognized.
  • These may occur in many forms of adenomas including somatotroph, lactotroph, mixed somatotroph and lactotroph, null cell/gonadotroph cell and, rarely, corticotroph cell adenomas.
  • [MeSH-major] Adenoma / metabolism. Biomarkers, Tumor / biosynthesis. Epitopes. Neurons / metabolism. Pituitary Neoplasms / metabolism
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / metabolism. ACTH-Secreting Pituitary Adenoma / pathology. Adult. Aged. Aged, 80 and over. Antibodies. Cell Differentiation. Female. Gonadotrophs / metabolism. Gonadotrophs / pathology. Human Growth Hormone / metabolism. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Staging. Prolactin / metabolism. Prolactinoma / metabolism. Prolactinoma / pathology. Retrospective Studies

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  • (PMID = 17875653.001).
  • [ISSN] 0022-1554
  • [Journal-full-title] The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
  • [ISO-abbreviation] J. Histochem. Cytochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Biomarkers, Tumor; 0 / Epitopes; 12629-01-5 / Human Growth Hormone; 9002-62-4 / Prolactin
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4. Lupi I, Manetti L, Caturegli P, Menicagli M, Cosottini M, Iannelli A, Acerbi G, Bevilacqua G, Bogazzi F, Martino E: Tumor infiltrating lymphocytes but not serum pituitary antibodies are associated with poor clinical outcome after surgery in patients with pituitary adenoma. J Clin Endocrinol Metab; 2010 Jan;95(1):289-96
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  • [Title] Tumor infiltrating lymphocytes but not serum pituitary antibodies are associated with poor clinical outcome after surgery in patients with pituitary adenoma.
  • CONTEXT: Serum pituitary antibodies (Pit Abs) and tumor-infiltrating lymphocytes (TILs) have been described in pituitary adenomas, but their clinical significance remains unknown.
  • OBJECTIVE: The objective of the study was to assess Pit Abs and TILs prevalence in pituitary adenomas and their influence on clinical outcome.
  • PATIENTS AND SETTING: Two hundred ninety-one pituitary adenoma cases (110 non-secreting, 30 ACTH-69 GH-71 prolactin- and 13 TSH-secreting adenoma; 177 operated and 114 untreated), 409 healthy controls, and 14 autoimmune hypophysitis were enrolled in a tertiary referral center.
  • The presence of TILs was evaluated using CD45 staining in a subset of adenomas surgically treated (n = 72).
  • MAIN OUTCOME MEASURE: Clinical response of pituitary adenoma after surgery was evaluated.
  • RESULTS: Pit Abs prevalence was higher in adenomas (5.1%) than healthy subjects (0.7%, P < 0.0001) and lower than in autoimmune hypophysitis patients (57%, P < 0.0001).
  • Similarly, TILs prevalence was higher in adenomas than normal pituitary (P = 0.01) and lower than in autoimmune hypophysitis (P < 0.0001).
  • A poor clinical outcome was more common in adenoma patients with TILs (11 of 18, 61%) than in those without (17 of 54, 31%, P = 0.026).
  • Multivariate regression analysis identified the presence of TILs as independent prognostic factor for persistence/recurrence of pituitary adenoma.
  • CONCLUSIONS: TILs and Pit Abs are present in a significant number of pituitary adenoma patients.
  • Cell-mediated immunity appears to be predictive of a less favorable clinical outcome.

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  • [Cites] Horm Res. 2001;55(6):288-92 [11805433.001]
  • [Cites] Pituitary. 2011 Dec;14(4):388-94 [19466616.001]
  • [Cites] Eur J Cancer. 2002 Oct;38(15):2014-9 [12376206.001]
  • [Cites] J Endocrinol. 2002 Nov;175(2):417-23 [12429039.001]
  • [Cites] Eur J Endocrinol. 2002 Dec;147(6):767-75 [12457452.001]
  • [Cites] N Engl J Med. 2003 Jan 16;348(3):203-13 [12529460.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Feb;88(2):650-4 [12574195.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jul 8;100(14):8372-7 [12826605.001]
  • [Cites] Endocr J. 2003 Dec;50(6):697-702 [14709840.001]
  • [Cites] Endocrine. 2003 Dec;22(3):335-40 [14709807.001]
  • [Cites] Lancet. 1987 Jun 20;1(8547):1394-8 [2884495.001]
  • [Cites] J Clin Endocrinol Metab. 1988 Oct;67(4):633-8 [3417843.001]
  • [Cites] J Endocrinol Invest. 1991 Sep;14(8):691-6 [1774454.001]
  • [Cites] Clin Endocrinol (Oxf). 1993 May;38(5):495-500 [8080469.001]
  • [Cites] Acta Neurochir (Wien). 1994;126(1):38-43 [8154320.001]
  • [Cites] J Clin Endocrinol Metab. 1995 Dec;80(12):3421-4 [8530576.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Feb;83(2):609-18 [9467582.001]
  • [Cites] J Lab Clin Med. 1998 Jul;132(1):25-31 [9665368.001]
  • [Cites] Endocr J. 1998 Jun;45(3):357-61 [9790270.001]
  • [Cites] Endocr Rev. 2005 Aug;26(5):599-614 [15634713.001]
  • [Cites] J Neurosurg. 2006 Aug;105(2):309-14 [17219839.001]
  • [Cites] J Clin Endocrinol Metab. 2007 Feb;92(2):604-7 [17090639.001]
  • [Cites] Neurol Med Chir (Tokyo). 2007 Mar;47(3):136-9 [17384498.001]
  • [Cites] J Thorac Oncol. 2006 Jul;1(6):513-9 [17409910.001]
  • [Cites] J Clin Endocrinol Metab. 2007 Jun;92(6):2176-81 [17341554.001]
  • [Cites] Ann N Y Acad Sci. 2007 Jun;1107:129-35 [17804540.001]
  • [Cites] J Endocrinol Invest. 2007 Sep;30(8):677-83 [17923800.001]
  • [Cites] Neurosurg Rev. 2008 Apr;31(2):157-63 [18253771.001]
  • [Cites] Endocr J. 2000 Aug;47(4):407-16 [11075721.001]
  • [Cites] Immunol Rev. 2008 Apr;222:101-16 [18363996.001]
  • [Cites] Immunol Rev. 2008 Apr;222:328-40 [18364012.001]
  • [Cites] Arch Immunol Ther Exp (Warsz). 2008 May-Jun;56(3):181-91 [18512029.001]
  • [Cites] Clin Endocrinol (Oxf). 2008 Aug;69(2):269-78 [18194487.001]
  • [Cites] Endocr J. 2008 Aug;55(4):729-35 [18497455.001]
  • [Cites] Am J Surg Pathol. 2008 Nov;32(11):1661-6 [18753941.001]
  • [Cites] Histochem Cell Biol. 2008 Dec;130(6):1079-90 [18953558.001]
  • [Cites] Cancer Immun. 2008;8:16 [19053167.001]
  • [Cites] Cancer Lett. 2009 Jun 18;278(2):123-9 [18930343.001]
  • [Cites] No Shinkei Geka. 2002 Jan;30(1):95-9 [11806114.001]
  • (PMID = 19875479.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R21 DK080351; United States / NIDDK NIH HHS / DK / DK080351
  • [Publication-type] Evaluation Studies; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / Biomarkers
  • [Other-IDs] NLM/ PMC2805498
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5. Evang JA, Borota OC, Melum E, Holm R, Ramm-Pettersen J, Bollerslev J, Berg JP: HDAC2 expression and variable number of repeats in exon 1 of the HDAC2 gene in corticotroph adenomas. Clin Endocrinol (Oxf); 2010 Aug;73(2):229-35
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HDAC2 expression and variable number of repeats in exon 1 of the HDAC2 gene in corticotroph adenomas.
  • OBJECTIVES: Alterations in protein expression of histone deacetylase 2 (HDAC2) have been demonstrated in various neoplasms, and lack of nuclear expression of HDAC2 has previously been shown in some human and canine corticotroph adenomas.
  • This study aimed to examine HDAC2 expression in a Norwegian cohort of corticotroph adenomas, screen for exonic HDAC2 gene variants in the adenomas and correlate the results with clinical data.
  • PATIENTS AND DESIGN: Forty-four patients with verified Cushing's disease or Nelson's syndrome, positive ACTH staining and tissue available for immunohistochemistry and/or DNA sequencing were included.
  • RESULTS: Histone deacetylase 2 expression examined by immunohistochemistry was strongly reduced in 3/30 adenomas.
  • A previously unidentified insertion of three bases in a region coding for a polyserine cluster in exon 1 of the HDAC2 gene was identified in 6/32 adenomas.
  • The same insertion was also found in 28/94 of the controls (i.e., not significantly different from the patients).
  • CONCLUSIONS: Strongly reduced HDAC2 protein expression was confirmed in a small portion of corticotroph tumours.
  • Mutations in HDAC2 exons are unlikely to play an important role in the development of corticotroph adenomas.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / genetics. Adenoma / genetics. Histone Deacetylase 2 / genetics. Minisatellite Repeats

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  • (PMID = 20346000.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.5.1.98 / HDAC2 protein, human; EC 3.5.1.98 / Histone Deacetylase 2
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6. Acosta-Gómez MJ, Muros MA, Llamas-Elvira JM, Ramírez A, Ortega S, Sabatel G, Ramos C, de la Riva-Aguilar A: The role of somatostatin receptor scintigraphy in patients with pituitary adenoma or post-surgical recurrent tumours. Br J Radiol; 2005 Feb;78(926):110-5
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  • [Title] The role of somatostatin receptor scintigraphy in patients with pituitary adenoma or post-surgical recurrent tumours.
  • To assess the role of scintigraphy with 111In-DTPA-D-Phe-octreotide (111In-octreotide) in the diagnosis of pituitary adenomas and in the evaluation of post-surgical recurrent or residual tumours, we performed scintigraphy with 111In-DTPA-D-Phe-octreotide (SRS) in 35 patients: 14 patients with confirmed pituitary tumours and 15 with confirmed recurrent tumours.
  • In the present study, scintigraphy with 111In-octreotide showed positive uptake in 10 out of 14 patients with confirmed pituitary tumour and in 13 out of 15 patients with confirmed recurrent tumour, with an overall sensitivity of 79%.
  • SRS showed better results in growth hormone (GH)- and prolactin (PRL)-secreting tumours (7/8 patients correctly identified) than in other adenomas (3/9).
  • SRS detected recurrence of adenocorticotrophic hormone (ACTH)-secreting tumours (4/5 patients correctly identified) and non-secreting tumours (5/7 patients correctly identified).
  • 111In-octreotide scintigraphy, in combination with other imaging modalities, is useful in the diagnosis and follow-up of pituitary tumours.
  • [MeSH-major] Adenoma / radionuclide imaging. Neoplasm Recurrence, Local / radionuclide imaging. Pentetic Acid / analogs & derivatives. Pituitary Neoplasms / radionuclide imaging. Radiopharmaceuticals. Receptors, Somatostatin
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Female. Follow-Up Studies. Humans. Magnetic Resonance Imaging / methods. Male. Middle Aged. Neoplasm, Residual. Postoperative Care. Prospective Studies. Tomography, X-Ray Computed / methods

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  • (PMID = 15681321.001).
  • [ISSN] 0007-1285
  • [Journal-full-title] The British journal of radiology
  • [ISO-abbreviation] Br J Radiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / (111)indium-DTPA-D-phe octreoide; 0 / Radiopharmaceuticals; 0 / Receptors, Somatostatin; 7A314HQM0I / Pentetic Acid
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7. Lad SP, Patil CG, Laws ER Jr, Katznelson L: The role of inferior petrosal sinus sampling in the diagnostic localization of Cushing's disease. Neurosurg Focus; 2007;23(3):E2
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  • [Title] The role of inferior petrosal sinus sampling in the diagnostic localization of Cushing's disease.
  • Cushing's syndrome can present a complex problem of differential diagnosis.
  • Of cases in which hypercortisolemia results from an adrenocorticotropic hormone (ACTH)-dependent process, approximately 80% are due to a pituitary adenoma (Cushing's disease [CD]), 10% are due to adrenal lesions, and the remaining 10% are secondary to ectopic ACTH secretion.
  • For patients with CD, surgical removal of the pituitary adenoma is the treatment of choice.
  • Thus, localization of the source of ACTH secretion is critical in guiding timely treatment decisions.
  • Inferior petrosal sinus sampling (IPSS) is considered to be the gold standard for confirming the origin of ACTH secretion in patients with Cushing's syndrome.
  • A number of other techniques are discussed including sampling from the cavernous sinus, the jugular vein, and multiple sites to aid the diagnosis and lateralization of ACTH-producing pituitary adenomas.
  • [MeSH-major] Petrosal Sinus Sampling / methods. Pituitary ACTH Hypersecretion / diagnosis

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  • (PMID = 17961020.001).
  • [ISSN] 1092-0684
  • [Journal-full-title] Neurosurgical focus
  • [ISO-abbreviation] Neurosurg Focus
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
  • [Number-of-references] 46
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8. Martínez-Fuentes AJ, Moreno-Fernández J, Vázquez-Martínez R, Durán-Prado M, de la Riva A, Tena-Sempere M, Diéguez C, Jiménez-Reina L, Webb SM, Pumar A, Leal-Cerro A, Benito-López P, Malagón MM, Castaño JP: Ghrelin is produced by and directly activates corticotrope cells from adrenocorticotropin-secreting adenomas. J Clin Endocrinol Metab; 2006 Jun;91(6):2225-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ghrelin is produced by and directly activates corticotrope cells from adrenocorticotropin-secreting adenomas.
  • CONTEXT: In Cushing's disease, ACTH hypersecretion by pituitary corticotrope adenoma cells and resulting hypercortisolism is accompanied by a severely blunted GH secretory response.
  • Interestingly, in Cushing's disease, ghrelin markedly increases plasma ACTH, whereas its stimulatory action on GH secretion is reduced.
  • Although the reported expression of ghrelin receptors (GHS-R) in corticotrope tumors offers a potential mechanism for ghrelin-induced ACTH hypersecretion, studies on the direct effects of synthetic GH secretagogues on corticotropinoma cells offered contradictory results.
  • OBJECTIVE AND DESIGN: To evaluate the direct action of ghrelin on corticotropinoma cells from two patients with Cushing's disease, we measured its effect on free cytosolic calcium concentration ([Ca(2+)](i)).
  • Additionally, expression of GHS-R and its ligand ghrelin was examined in these cells and in five additional corticotropinomas.
  • RESULTS: Ghrelin (10(-6) m) induced a marked [Ca(2+)](i) increase in 89.5% (case 1; n = 19 cells) and 85% (case 2; n = 13 cells) of corticotropinoma cells.
  • Moreover, RT-PCR showed that expression of GHS-R isoforms is accompanied by that of ghrelin in all seven corticotrope adenomas examined.
  • Importantly, double immunogold electron microscopy revealed that ghrelin is costored within ACTH secretory vesicles in densely granulated adenomatous corticotropes.
  • CONCLUSIONS: These results constitute the first demonstration that ghrelin acts directly on corticotrope tumor cells derived from patients with Cushing's disease.
  • The presence of ghrelin and GHS-R suggests that pituitary ghrelin may play an autocrine/paracrine role in regulating ACTH release in Cushing's disease.
  • Our findings provide a plausible cellular basis for the exaggerated ACTH response to ghrelin in Cushing's disease and suggest novel research strategies to develop medical treatments for this disease.
  • [MeSH-major] Adenoma / secretion. Adrenocorticotropic Hormone / secretion. Peptide Hormones / physiology. Pituitary Neoplasms / secretion

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  • (PMID = 16551736.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ghrelin; 0 / Peptide Hormones; 0 / RNA, Messenger; 0 / Receptors, G-Protein-Coupled; 0 / Receptors, Ghrelin; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; SY7Q814VUP / Calcium
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9. Assie G, Louiset E, Sturm N, René-Corail F, Groussin L, Bertherat J, Thomas M, Lefebvre H, Feige JJ, Clauser E, Chabre O, Cherradi N: Systematic analysis of G protein-coupled receptor gene expression in adrenocorticotropin-independent macronodular adrenocortical hyperplasia identifies novel targets for pharmacological control of adrenal Cushing's syndrome. J Clin Endocrinol Metab; 2010 Oct;95(10):E253-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Systematic analysis of G protein-coupled receptor gene expression in adrenocorticotropin-independent macronodular adrenocortical hyperplasia identifies novel targets for pharmacological control of adrenal Cushing's syndrome.
  • CONTEXT: Stimulation of cortisol secretion through abnormally expressed G protein-coupled receptors (GPCRs) is a frequent feature of ACTH-independent macronodular adrenal hyperplasia (AIMAH).
  • This has opened a pharmacological strategy that targets GPCRs for the treatment of Cushing's syndrome in AIMAH.
  • OBJECTIVE: The objective of the study was to identify new GPCR targets for the pharmacological treatment of adrenal Cushing's syndrome.
  • DESIGN AND PATIENTS: We designed a cDNA chip containing 865 nucleotidic sequences of GPCRs. mRNAs were extracted from three normal adrenals, 18 AIMAHs, four adrenals from Cushing's disease patients, and 13 cortisol-secreting adenomas.
  • RESULTS: The ACTH MC2 receptor showed a low expression in 15 of 18 AIMAHs samples, whereas several previously undescribed GPCR genes were found highly expressed in a subset of AIMAH, such as the receptors for motilin (MLNR; three of 18 AIMAHs) and γ-aminobutyric acid (GABBR1; five of 18 AIMAHs), and the α2A adrenergic receptor (ADRA2A; 13 of 18 AIMAHs), on which we focused our attention.
  • Western blot and immunochemistry analyses showed expression of ADRA2A protein in AIMAH but not in normal adrenal cortex.
  • CONCLUSION: ADRA2A is a potential target for pharmacological treatment of Cushing's syndrome linked to AIMAH.
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / genetics. ACTH-Secreting Pituitary Adenoma / pathology. Adrenergic alpha-2 Receptor Agonists. Adrenocorticotropic Hormone / metabolism. Adrenocorticotropic Hormone / physiology. Antihypertensive Agents / administration & dosage. Antihypertensive Agents / pharmacology. Cells, Cultured. Clonidine / administration & dosage. Clonidine / pharmacology. Gene Expression. Gene Expression Profiling. Humans. Hyperplasia / genetics. Hyperplasia / metabolism. Oligonucleotide Array Sequence Analysis. Pituitary Neoplasms / genetics. Pituitary Neoplasms / pathology. Receptors, Adrenergic, alpha-2 / genetics. Receptors, Adrenergic, alpha-2 / metabolism. Receptors, Adrenergic, alpha-2 / physiology


10. Pisarek H, Pawlikowski M, Kunert-Radek J, Radek M: Expression of somatostatin receptor subtypes in human pituitary adenomas -- immunohistochemical studies. Endokrynol Pol; 2009 Jul-Aug;60(4):240-51
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  • [Title] Expression of somatostatin receptor subtypes in human pituitary adenomas -- immunohistochemical studies.
  • BACKGROUND: The highly variable expression of SSTR subtypes in pituitary adenomas (PA) may partially explain why the subgroup of somatotropinomas or other adenomas do not respond to the therapeutic action of currently used long-acting somatostatin analogues like octreotide or lanreotide.
  • RESULTS: The pattern of SSTR immunostaining (estimated according to the percentage frequency of appearance) was in acromegaly: SSTR 5 > SSTR 1 > SSTR 2A = SSTR 3 > SSTR 2B, in prolactinomas: SSTR 2B = SSTR 3 = SSTR 5 > SSTR 1 = SSTR 2A, in gonadotropinomas: SSTR 3 > SSTR 2B > SSTR 1 = SSTR 2A > SSTR 5, in corticotropinomas: SSTR 2A > SSTR 1 = SSTR 3 > SSTR 5 > SSTR 2B.
  • In PA immunonegative for pituitary hormones, we noticed only a weak staining of all receptor subtypes including SSTR 4.
  • In plurihormonal adenomas with positive GH phenotype the staining pattern was: SSTR 5 > SSTR 1 = SSTR 2B and in plurihormonal PA with negative GH phenotype: SSTR 1 = SSTR 5 > SSTR 2A = SSTR 2B = SSTR 3.
  • In plurihormonal adenoma with ACTH immunopositivity, the staining pattern was: SSTR = SSTR 2A = SSTR 3 = SSTR 5.
  • SSTR 1 and SSTR 5 were the most frequent subtypes of somatostatin receptor in plurihormonal adenomas without ACTH expression.
  • Apart from applying SSTR 2 and SSTR 5-preferring octreotide and lanreotide - newly synthesized multiligand analogues, such as SOM 230, KE 108, or other SST selective analogues, may represent a further useful approach for the treatment, especially in cases other than somatotropinoma or thyrotropinoma.
  • [MeSH-major] Adenoma / metabolism. Pituitary Neoplasms / metabolism. Receptors, Somatostatin / metabolism

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  • (PMID = 19753537.001).
  • [ISSN] 0423-104X
  • [Journal-full-title] Endokrynologia Polska
  • [ISO-abbreviation] Endokrynol Pol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Peptides, Cyclic; 0 / Protein Isoforms; 0 / Receptors, Somatostatin; 0G3DE8943Y / lanreotide; 51110-01-1 / Somatostatin; RWM8CCW8GP / Octreotide
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11. Cooper O, Ben-Shlomo A, Bonert V, Bannykh S, Mirocha J, Melmed S: Silent corticogonadotroph adenomas: clinical and cellular characteristics and long-term outcomes. Horm Cancer; 2010 Apr;1(2):80-92
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  • [Title] Silent corticogonadotroph adenomas: clinical and cellular characteristics and long-term outcomes.
  • Silent corticotrophins adenomas (SCAs) are clinically silent and non-secreting but immunostain positively for ACTH.
  • We hypothesize that SCAs comprise both corticotroph and gonadotroph characteristics.
  • We compared preoperative and postoperative clinical results and tumor cytogenesis in 25 SCAs and 84 nonfunctioning adenomas in 109 consecutive patients diagnosed pre-operatively with nonfunctioning pituitary adenomas.
  • Pathologic outcomes were expression of relevant pituitary hormones, tissue-specific transcription factors, and electron microscopy features.
  • Preoperative SCA presentation was similar to that observed for nonfunctioning adenomas.
  • However, SCAs recurred postoperatively at a median of 3 years vs. 8 years for nonfunctioning adenomas (p<0.0001).
  • Fifty-four percent of patients with SCAs had new onset postoperative hypopituitarism vs. 17% of nonfunctioning adenomas (p<0.025).
  • SCAs (n=18) were immunopositive for ACTH, cytoplasmic and nuclear SF-1, NeuroD1, DAX-1, and alpha-gonadotropin subunit, but Tpit negative, and co-expression of tumor ACTH with either SF-1 or LH was detected.
  • In contrast, functional corticotroph adenomas (n=11) were immunopositive for ACTH, nuclear SF-1, NeuroD1, and Tpit, but negative for DAX-1, a gonadotroph cell transcription factor.
  • Gonadotroph adenomas (n=23) were immunonegative for ACTH and Tpit but positive for nuclear SF-1, NeuroD1, and DAX-1.
  • SCA electron microscopy demonstrated ultrastructural features consistent with corticotroph and gonadotroph cells.
  • As SCAs exhibit features consistent with both corticotroph and gonadotroph cytologic origin, we propose a pathologic and clinically distinct classification of SCAs as silent corticogonadotroph adenomas.

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  • [Cites] J Clin Endocrinol Metab. 2000 Jul;85(7):2537-42 [10902805.001]
  • [Cites] Clin Endocrinol (Oxf). 1998 May;48(5):647-54 [9666878.001]
  • [Cites] Cell. 2001 Mar 23;104(6):849-59 [11290323.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Jun;86(6):2476-83 [11397843.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Jul 17;98(15):8674-9 [11447259.001]
  • [Cites] Mod Pathol. 2001 Sep;14(9):892-9 [11557786.001]
  • [Cites] Acta Neuropathol. 2001 Oct;102(4):398-403 [11603817.001]
  • [Cites] Neuropathology. 2001 Dec;21(4):288-93 [11837535.001]
  • [Cites] Endocr Pathol. 2002 Summer;13(2):125-30 [12165660.001]
  • [Cites] Endocr J. 2002 Jun;49(3):285-92 [12201210.001]
  • [Cites] Clin Endocrinol (Oxf). 2003 Jan;58(1):59-64 [12519413.001]
  • [Cites] Genes Dev. 2003 Mar 15;17(6):738-47 [12651892.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Jul;88(7):3050-6 [12843142.001]
  • [Cites] Pituitary. 2002;5(4):221-3 [14558669.001]
  • [Cites] Neurosurgery. 2003 Nov;53(5):1076-84; discussion 1084-5 [14580274.001]
  • [Cites] J Clin Invest. 2003 Dec;112(11):1603-18 [14660734.001]
  • [Cites] Endocr Pathol. 2003 Winter;14(4):363-8 [14739492.001]
  • [Cites] Hum Pathol. 2004 Sep;35(9):1137-47 [15343517.001]
  • [Cites] Am J Pathol. 1980 Mar;98(3):617-38 [6244736.001]
  • [Cites] J Pathol. 1985 Jan;145(1):59-62 [3881578.001]
  • [Cites] J Neurosurg. 1987 Feb;66(2):244-50 [3543255.001]
  • [Cites] Virchows Arch A Pathol Anat Histopathol. 1988;413(1):61-8 [2453972.001]
  • [Cites] Acta Endocrinol (Copenh). 1988 Aug;118(4):533-7 [2840793.001]
  • [Cites] Pathol Res Pract. 1988 Sep;183(5):601-5 [2467268.001]
  • [Cites] Pathol Res Pract. 1988 Sep;183(5):610-2 [2467270.001]
  • [Cites] Neurosurgery. 1990 Mar;26(3):397-403 [1690866.001]
  • [Cites] Am J Pathol. 1990 Aug;137(2):479-88 [2167013.001]
  • [Cites] Virchows Arch A Pathol Anat Histopathol. 1990;417(4):361-7 [2173251.001]
  • [Cites] Hum Pathol. 1991 Jul;22(7):719-21 [1649119.001]
  • [Cites] Pathol Res Pract. 1991 Jun;187(5):637-41 [1717963.001]
  • [Cites] Neurol Med Chir (Tokyo). 1992;32(7 Spec No):381-547 [1381065.001]
  • [Cites] Ultrastruct Pathol. 1999 May-Jun;23(3):141-8 [10445280.001]
  • [Cites] Mol Endocrinol. 1999 Aug;13(8):1267-84 [10446902.001]
  • [Cites] Br J Neurosurg. 2005 Feb;19(1):38-42 [16147581.001]
  • [Cites] Endocr Pathol. 2005 Fall;16(3):239-44 [16299407.001]
  • [Cites] Pathol Res Pract. 2006;202(6):457-64 [16497445.001]
  • [Cites] Neurosurgery. 2006 Aug;59(2):341-53; discussion 341-53 [16883174.001]
  • [Cites] Clin Genet. 2007 Sep;72(3):175-82 [17718852.001]
  • [Cites] Neurosurgery. 2007 Sep;61(3):580-4; discussion 584-5 [17881972.001]
  • [Cites] Exp Clin Endocrinol Diabetes. 2007 Oct;115(9):610-5 [17943697.001]
  • [Cites] Eur J Endocrinol. 2007 Dec;157(6):717-24 [18057378.001]
  • [Cites] Endocr J. 2007 Dec;54(6):961-8 [18079591.001]
  • [Cites] J Clin Endocrinol Metab. 2008 May;93(5):1526-40 [18334580.001]
  • [Cites] Mol Endocrinol. 2008 Jul;22(7):1647-57 [18388149.001]
  • [Cites] Neuro Endocrinol Lett. 2008 Jun;29(3):347-50 [18580839.001]
  • [Cites] Endocr Pathol. 2008 Spring;19(1):17-26 [18228160.001]
  • [Cites] Clin Endocrinol (Oxf). 2010 May;72(5):648-53 [19650787.001]
  • [Cites] Pathol Int. 1994 Sep;44(9):697-703 [7804432.001]
  • [Cites] Eur J Endocrinol. 1995 Jul;133(1):25-32 [7542980.001]
  • [Cites] J Clin Endocrinol Metab. 1996 Jun;81(6):2165-70 [8964846.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Mar;82(3):818-24 [9062489.001]
  • [Cites] Endocr J. 1997 Apr;44(2):329-33 [9228470.001]
  • [Cites] Clin Endocrinol (Oxf). 1997 Jun;46(6):669-79 [9274697.001]
  • [Cites] Mol Cell Biol. 1997 Nov;17(11):6673-82 [9343431.001]
  • [Cites] Endocrinol Metab Clin North Am. 1997 Dec;26(4):741-62 [9429858.001]
  • [Cites] Neurosurgery. 2000 Sep;47(3):723-9; discussion 729-30 [10981760.001]
  • (PMID = 20717480.001).
  • [ISSN] 1868-8500
  • [Journal-full-title] Hormones & cancer
  • [ISO-abbreviation] Horm Cancer
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / T32 DK007770-08; United States / NCI NIH HHS / CA / R01 CA075979-08; United States / NIDDK NIH HHS / DK / T32 DK007770; United States / NIDDK NIH HHS / DK / T32 DK07770; United States / NIDDK NIH HHS / DK / DK007770-08; United States / NCI NIH HHS / CA / CA 075979; United States / NCI NIH HHS / CA / R01 CA075979; United States / NCI NIH HHS / CA / CA075979-08
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gonadotropins
  • [Keywords] NOTNLM ; Corticotroph adenoma / Gonadotroph adenoma / Nonfunctioning adenoma / Pituitary adenoma
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12. Segal-Lieberman G, Rubinfeld H, Glick M, Kronfeld-Schor N, Shimon I: Melanin-concentrating hormone stimulates human growth hormone secretion: a novel effect of MCH on the hypothalamic-pituitary axis. Am J Physiol Endocrinol Metab; 2006 May;290(5):E982-8
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  • [Title] Melanin-concentrating hormone stimulates human growth hormone secretion: a novel effect of MCH on the hypothalamic-pituitary axis.
  • It is cleaved from its precursor prepro-MCH (ppMCH) along with several other neuropeptides whose roles are not fully defined.
  • Because pituitary hormones such as growth hormone (GH), ACTH, and thyroid-stimulating hormone affect body weight and composition, appetite, insulin sensitivity, and lipoprotein metabolism, we investigated whether MCH exerts direct effects on the human pituitary to regulate energy balance using dispersed human fetal pituitaries (21-22 wk gestation) and cultured GH-secreting adenomas.
  • We found that MCH receptor-1 (MCH-R1), but not MCH receptor-2, is expressed in both normal (fetal and adult) human pituitary tissues and in GH cell adenomas.
  • MCH (10 nM) stimulated GH release from human fetal pituitary cultures by up to 62% during a 4-h incubation (P < 0.05).
  • A milder, albeit significant, induction of GH secretion by MCH (20%) was seen in cultured GH-secreting pituitary adenomas.
  • A comparable stimulation of GH secretion was seen when cultured mouse pituitary cells were treated with MCH.
  • Treatment of cultured GH adenoma cells with MCH (100 nM) induced extracellular signal-regulated kinases 1 and 2 phosphorylation, suggesting activation of MCH-R1.
  • In aggregate, these data suggest that MCH may regulate pituitary GH secretion and imply a potential cross-talk mechanism between appetite-regulating neuropeptides and pituitary hormones.
  • [MeSH-major] Human Growth Hormone / secretion. Hypothalamic Hormones / pharmacology. Hypothalamo-Hypophyseal System / drug effects. Melanins / pharmacology. Pituitary Hormones / pharmacology
  • [MeSH-minor] Animals. Cells, Cultured. Fetus. Gene Expression / genetics. Growth Hormone-Releasing Hormone / pharmacology. Humans. Mice. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Oligopeptides / pharmacology. Phosphorylation / drug effects. Pituitary Gland / cytology. Pituitary Gland / metabolism. Pituitary Neoplasms / metabolism. Pituitary Neoplasms / pathology. Receptors, Somatostatin / genetics. Tumor Cells, Cultured

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  • (PMID = 16603725.001).
  • [ISSN] 0193-1849
  • [Journal-full-title] American journal of physiology. Endocrinology and metabolism
  • [ISO-abbreviation] Am. J. Physiol. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hypothalamic Hormones; 0 / MCHR1 protein, human; 0 / Melanins; 0 / Oligopeptides; 0 / Pituitary Hormones; 0 / Receptors, Somatostatin; 0 / neuropeptide EI; 12629-01-5 / Human Growth Hormone; 67382-96-1 / melanin-concentrating hormone; 9034-39-3 / Growth Hormone-Releasing Hormone; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
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13. Jagannathan J, Sheehan JP, Pouratian N, Laws ER, Steiner L, Vance ML: Gamma Knife surgery for Cushing's disease. J Neurosurg; 2007 Jun;106(6):980-7
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  • [Title] Gamma Knife surgery for Cushing's disease.
  • OBJECT: In this study the authors address the efficacy and safety of Gamma Knife surgery (GKS) in patients with adrenocorticotropic hormone-secreting pituitary adenomas.
  • METHODS: A review of data collected from a prospective GKS database between January 1990 and March 2005 was performed in patients with Cushing's disease.
  • All but one patient underwent resection for a pituitary tumor, without achieving remission.
  • Patient records were also evaluated for changes in tumor volume, development of new hormone deficiencies, visual acuity, cranial nerve neuropathies, and radiation-induced imaging changes.
  • The mean dose, to the tumor margin was 23 Gy (median 25 Gy).
  • In the 49 patients in whom a tumor was visible on the planning magnetic resonance (MR) image, a decrease in tumor size occurred in 39 (80%), in seven patients there was to change in size, and tumor growth occurred in three patients.
  • Ten patients (20%) experienced a relapse of Cushing's disease after initial remission; the mean time to recurrence was 27 months (range 6-60 months).
  • CONCLUSIONS: Gamma Knife surgery is an effective treatment for persistent Cushing's disease.
  • Adenomas with cavernous sinus invasion that are not amenable to resection are treatable with the Gamma Knife.
  • These results demonstrate the value of combining two neurosurgical treatment modalities-microsurgical resection and GKS-in the management of pituitary adenomas.
  • [MeSH-major] Pituitary ACTH Hypersecretion / surgery. Pituitary Neoplasms / surgery. Radiosurgery
  • [MeSH-minor] Adrenocorticotropic Hormone / metabolism. Cranial Nerve Injuries / etiology. Endocrine System Diseases / etiology. Follow-Up Studies. Humans. Magnetic Resonance Imaging. Neoplasm Recurrence, Local. Retrospective Studies. Treatment Outcome. Vision Disorders / etiology

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  • [CommentIn] J Neurosurg. 2007 Jun;106(6):976-7; discussion 977-9 [17564167.001]
  • (PMID = 17564168.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
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14. Bezerra MG, Latronico AC, Fragoso MC: [Endocrine tumors associated to protein Gsalpha/Gi2alpha mutations]. Arq Bras Endocrinol Metabol; 2005 Oct;49(5):784-90
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  • Many oncogenic mutations promote tumor growth by inducing autonomous activity of proteins that normally transmit proliferative signal initiated by extracellular factors.
  • The G proteins couple an array of seven transmembrane receptors at the cell surface with a variety of intracellular effectors, which produce second messenger molecules.
  • A subset of endocrine tumors, such as GH- or ACTH-secreting pituitary adenomas, functioning thyroid adenomas, adrenocortical and gonadal tumors were associated with somatic activating mutations in the highly conserved codons of the Gs (Arg201 and Gln227) and Gi (Arg179 and Gln205) proteins.
  • [MeSH-major] Endocrine Gland Neoplasms / genetics. GTP-Binding Protein alpha Subunits, Gi-Go / genetics. GTP-Binding Protein alpha Subunits, Gs / genetics. Mutation / genetics. Oncogenes / genetics

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  • (PMID = 16444361.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] por
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Brazil
  • [Chemical-registry-number] EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gi-Go; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs
  • [Number-of-references] 64
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15. Min HS, Lee SJ, Kim SK, Park SH: Pituitary adenoma with rich folliculo-stellate cells and mucin-producing epithelia arising in a 2-year-old girl. Pathol Int; 2007 Sep;57(9):600-5
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  • [Title] Pituitary adenoma with rich folliculo-stellate cells and mucin-producing epithelia arising in a 2-year-old girl.
  • Pituitary adenoma is a rare neoplasm in childhood, with prolactin and adrenocorticotropic hormone (ACTH)-secreting adenomas predominating in this age group.
  • Herein is reported a case of an ACTH-producing macroadenoma with an unusual histology that occurred in a 2-year-old girl.
  • Because of the patient's age and the macroadenoma's suprasellar location and large size (up to 4 cm in diameter), radical surgery was performed under the suspicion of craniopharyngioma or germ-cell tumor.
  • Pathologically, it was a unique pituitary adenoma composed of monotonous ACTH-producing cells, smaller folliculo-stellate cells (FSC), and mucin-producing cells.
  • The FSC, non-hormone-secreting pituitary cells of uncertain function, were confirmed by their S-100 protein, glial fibrillary acidic protein and cytokeratin expression immunoprofiles.
  • The abrupt transition between the prominent gland-forming mucin-producing epithelia and the FSC component suggested that the mucin-producing epithelia might be derived from the FSC.
  • This association might represent so-called 'retrodifferentiation' of adenoma cells to the FSC and the precursor cells of Rathke's pouch.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / pathology. Mucins / secretion. Pituitary Neoplasms / pathology
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Child, Preschool. Cytoplasm / ultrastructure. Disease Progression. Female. Glial Fibrillary Acidic Protein / metabolism. Humans. Keratins / metabolism. Magnetic Resonance Imaging. S100 Proteins / metabolism. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 17685932.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Glial Fibrillary Acidic Protein; 0 / Mucins; 0 / S100 Proteins; 68238-35-7 / Keratins
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16. de Bruin C, Meij BP, Kooistra HS, Hanson JM, Lamberts SW, Hofland LJ: Cushing's disease in dogs and humans. Horm Res; 2009 Jan;71 Suppl 1:140-3
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  • [Title] Cushing's disease in dogs and humans.
  • BACKGROUND: Cushing's disease (CD) is a common endocrinological disorder in dogs with an estimated incidence of 1 to 2 cases/1,000 dogs/year.
  • Canine CD may therefore serve as an animal model for human CD, especially since therapeutic canine hypophysectomy can generate substantial amounts of primary corticotroph adenoma tissue for in vitro research purposes.
  • In a recent study, we found that dopamine (DA) D(2) and somatostatin (SS) receptor subtypes are well expressed in canine corticotroph adenomas, but there are some distinct differences compared with the expression profile observed in human CD.
  • CASE REPORT: This case involves an 8-year-old female dog that developed signs of exercise intolerance, muscle weakness and polyuria/polydipsia due to an adrenocorticotropic hormone-secreting pituitary adenoma.
  • [MeSH-major] Dog Diseases / radiography. Pituitary ACTH Hypersecretion / radiography. Pituitary ACTH Hypersecretion / veterinary

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19153526.001).
  • [ISSN] 1423-0046
  • [Journal-full-title] Hormone research
  • [ISO-abbreviation] Horm. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
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17. Izumoto S, Arita N: [Treatment of pituitary adenomas: recent topics]. No Shinkei Geka; 2010 Jan;38(1):79-89
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  • [Title] [Treatment of pituitary adenomas: recent topics].
  • [MeSH-major] Pituitary Neoplasms / therapy
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / therapy. Female. Humans. Male. Prolactinoma / therapy

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  • (PMID = 20085107.001).
  • [ISSN] 0301-2603
  • [Journal-full-title] No shinkei geka. Neurological surgery
  • [ISO-abbreviation] No Shinkei Geka
  • [Language] jpn
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 52
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18. de Bruin C, Feelders RA, Waaijers AM, van Koetsveld PM, Sprij-Mooij DM, Lamberts SW, Hofland LJ: Differential regulation of human dopamine D2 and somatostatin receptor subtype expression by glucocorticoids in vitro. J Mol Endocrinol; 2009 Jan;42(1):47-56
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Dopamine agonists (DA) and somatostatin (SS) analogues have been proposed in the treatment of ACTH-producing neuro-endocrine tumours that cause Cushing's syndrome.
  • In this study, we investigated the effects of the GC dexamethasone (DEX) on D(2) and sst expression in three human neuro-endocrine cell lines: BON (carcinoid) and TT (medullary thyroid carcinoma) versus DMS (small cell lung cancer), which is severely GC resistant.
  • In DMS, DEX did not cause significant changes in the expression of these receptor subtypes.
  • In conclusion, we show that GCs selectively down-regulate sst(2), but not D(2) and only to a minor degree sst(5) in human neuro-endocrine BON and TT cells.
  • This mechanism may also be responsible for the low expression of sst(2) in corticotroph adenomas and underwrite the current interest in sst(5) and D(2) as possible therapeutic targets for a medical treatment of Cushing's disease.
  • [MeSH-minor] Animals. Antineoplastic Agents, Hormonal / metabolism. Cell Line. Cell Proliferation. DNA Fragmentation. Dexamethasone / metabolism. Dopamine / metabolism. Hormone Antagonists / metabolism. Humans. Mifepristone / metabolism. Octreotide / metabolism. RNA, Messenger / metabolism. Radioligand Assay. Somatostatin / metabolism

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  • (PMID = 18852217.001).
  • [ISSN] 1479-6813
  • [Journal-full-title] Journal of molecular endocrinology
  • [ISO-abbreviation] J. Mol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Glucocorticoids; 0 / Hormone Antagonists; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin; 320T6RNW1F / Mifepristone; 51110-01-1 / Somatostatin; 7S5I7G3JQL / Dexamethasone; RWM8CCW8GP / Octreotide; VTD58H1Z2X / Dopamine
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19. Minniti G, Osti M, Jaffrain-Rea ML, Esposito V, Cantore G, Maurizi Enrici R: Long-term follow-up results of postoperative radiation therapy for Cushing's disease. J Neurooncol; 2007 Aug;84(1):79-84
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  • [Title] Long-term follow-up results of postoperative radiation therapy for Cushing's disease.
  • OBJECTIVES: Radiotherapy is currently used in patients with residual or recurrent pituitary adenomas after surgery.
  • However, there is little information of long-term outcome of patients with Cushing's disease following radiotherapy.
  • We assessed the long-term efficacy and toxicity of conventional radiotherapy in the control of Cushing's disease after unsuccessful transsphenoidal surgery.
  • PATIENTS AND METHODS: Forty patients with Cushing's disease were treated with conventional external beam radiotherapy at our Institution between 1988 and 2002.
  • The persistence of active disease after surgery was diagnosed by the increased high plasma cortisol levels, high 24 h urinary cortisol levels and absence of cortisol suppression after administration of dexamethasone.
  • CONCLUSION: Radiotherapy is effective in the long-term tumour- and hormone hypersecretion control of ACTH-secreting pituitary adenomas, however with a high prevalence of hypopituitarism.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / radiotherapy. Adenoma / radiotherapy. Neoplasm Recurrence, Local / radiotherapy. Neoplasm, Residual / radiotherapy. Pituitary ACTH Hypersecretion / radiotherapy
  • [MeSH-minor] Adult. Disease-Free Survival. Female. Follow-Up Studies. Humans. Hydrocortisone / blood. Male. Middle Aged

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  • [Cites] Clin Endocrinol (Oxf). 2005 Feb;62(2):210-6 [15670198.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Jan;83(1):63-7 [9435417.001]
  • [Cites] N Engl J Med. 1997 Jan 16;336(3):172-7 [8988897.001]
  • [Cites] Neurosurgery. 2001 Aug;49(2):284-91; discussion 291-2 [11504104.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Oct;85(10):3779-85 [11061538.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Feb;90(2):800-4 [15562021.001]
  • [Cites] J Neurooncol. 2000 Jun;48(2):135-40 [11083077.001]
  • [Cites] Neurosurgery. 2002 Jul;51(1):57-61; discussion 61-2 [12182435.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1994 Oct 15;30(3):557-65 [7928486.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Dec;89(12):6348-57 [15579802.001]
  • [Cites] J Clin Endocrinol Metab. 1992 Sep;75(3):935-42 [1517389.001]
  • [Cites] Clin Endocrinol (Oxf). 1990 Oct;33(4):445-55 [2225489.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Nov;87(11):4892-9 [12414846.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Dec;88(12):5593-602 [14671138.001]
  • [Cites] Clin Endocrinol (Oxf). 2002 Dec;57(6):713-7 [12460319.001]
  • [Cites] Ann Intern Med. 1988 Sep 15;109(6):487-93 [2843068.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1997 Mar 15;37(5):1031-4 [9169809.001]
  • [Cites] J Neurosurg. 2000 Nov;93(5):738-42 [11059652.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1995 Sep 30;33(2):307-14 [7673017.001]
  • [Cites] Clin Endocrinol (Oxf). 1993 Jun;38(6):571-8 [8334743.001]
  • [Cites] Acta Endocrinol (Copenh). 1986 Jul;112(3):310-4 [3529780.001]
  • [Cites] N Engl J Med. 1995 Mar 23;332(12):791-803 [7862184.001]
  • [Cites] Clin Endocrinol (Oxf). 2004 Nov;61(5):531-43 [15521954.001]
  • [Cites] J Neurosurg. 2002 Dec;97(5 Suppl):422-8 [12507068.001]
  • [Cites] J Neurooncol. 2000 Mar;47(1):79-84 [10930104.001]
  • [Cites] J Clin Endocrinol Metab. 1995 Nov;80(11):3114-20 [7593411.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Jan;88(1):34-7 [12519825.001]
  • [Cites] Clin Endocrinol (Oxf). 1985 Feb;22(2):169-77 [3921294.001]
  • [Cites] Clin Endocrinol (Oxf). 1989 Sep;31(3):309-23 [2559823.001]
  • (PMID = 17356896.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] WI4X0X7BPJ / Hydrocortisone
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20. Giacomini D, Haedo M, Gerez J, Druker J, Páez-Pereda M, Labeur M, Stalla GK, Arzt E: Differential gene expression in models of pituitary prolactin-producing tumoral cells. Horm Res; 2009 Apr;71 Suppl 2:88-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential gene expression in models of pituitary prolactin-producing tumoral cells.
  • Although several genes and signalling pathways have been identified as important effectors in the development of pituitary tumours, our understanding of pituitary tumorigenesis remains incomplete and is the focus of much current research.
  • Use of the mRNA differential display technique in prolactinomas from D2-receptor knockout mice and in stable GH3 cell line clones with enhanced tumorigenicity in vivo has led to the identification of two genes that are involved in the pathogenic process--BMP-4 and RSUME.
  • In contrast, BMP-4 has an inhibitory role in corticotrophinomas.
  • RSUME (RWD-containing sumoylation enhancer) was identified from a transformed lactosomatotrophic cell line that had increased tumorigenic and angiogenic potential.
  • The differential expression and action of BMP-4 in prolactinomas and corticotrophinomas highlights the importance of studying a gene with contrasting actions in two cell lineages of the same organ in order to understand the pituitary transformation process.
  • Both BMP-4 and RSUME may be interesting targets for inhibiting steps involved in pituitary tumorigenesis.
  • [MeSH-major] Bone Morphogenetic Protein 4 / biosynthesis. Gene Expression Regulation, Neoplastic. Models, Biological. Neoplasm Proteins / biosynthesis. Prolactinoma / metabolism. Transcription Factors / biosynthesis
  • [MeSH-minor] Animals. Cell Hypoxia / genetics. Cell Line, Tumor. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Gene Expression Profiling. Humans. Mice. Mice, Knockout. Receptors, Dopamine D2 / genetics. Receptors, Dopamine D2 / metabolism. Signal Transduction / genetics

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19407504.001).
  • [ISSN] 1423-0046
  • [Journal-full-title] Hormone research
  • [ISO-abbreviation] Horm. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / BMP4 protein, human; 0 / Bone Morphogenetic Protein 4; 0 / Neoplasm Proteins; 0 / RSUME protein, human; 0 / Receptors, Dopamine D2; 0 / Transcription Factors
  • [Number-of-references] 56
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21. Winczyk K, Pawlikowski M: Immunohistochemical detection of PPARgamma receptors in the human pituitary adenomas: correlation with PCNA. Folia Histochem Cytobiol; 2005;43(3):137-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunohistochemical detection of PPARgamma receptors in the human pituitary adenomas: correlation with PCNA.
  • The occurrence of peroxisome proliferator-activated receptors gamma (PPARgamma) was investigated in 51 human pituitary adenomas and in 6 non-tumoral human pituitary tissue samples.
  • The mean percentage of cells with positive nuclear reaction was 3-fold higher in pituitary adenomas in comparison with non-tumoral pituitary tissues.
  • It was clearly stronger in pituitary adenomas than in non-tumoral pituitary tissues.
  • A slight, statistically insignificant tendency towards negative correlation between PPARgamma and PCNA was found in somatotropinomas, prolactinomas, corticotropinomas and gonadotropinomas.
  • On the other hand, in null cell adenomas and "silent" corticotropinomas, a strong positve correlation between the expression of PPARgamma and PCNA was observed.
  • The strong expression of PPARgamma in human pituitary adenomas and its possible involvement in control of cell proliferation in these tumors give a good reason for the attempts of their treatment with PPARgamma ligands.

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  • (PMID = 16201313.001).
  • [ISSN] 0239-8508
  • [Journal-full-title] Folia histochemica et cytobiologica
  • [ISO-abbreviation] Folia Histochem. Cytobiol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / PPAR gamma; 0 / Proliferating Cell Nuclear Antigen
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22. de Herder WW, Kwekkeboom DJ, Valkema R, Feelders RA, van Aken MO, Lamberts SW, van der Lely AJ, Krenning EP: Neuroendocrine tumors and somatostatin: imaging techniques. J Endocrinol Invest; 2005;28(11 Suppl International):132-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The sensitivity of 111In-pentetreotide scintigraphy for the detection of gastrinomas, vasoactive intestinal polypeptide-secreting tumors, and glucagonomas as well as clinically non-functioning lesions is 75-100%.
  • Most GH- and TSH-secreting pituitary adenomas can be visualized using 111In-pentetreotide.
  • 111In-pentetreotide scintigraphy is negative in microprolactinomas and ACTH-secreting pituitary microadenomas.
  • 111In-pentetreotide scintigraphy has been successful for the localization of extra-pituitary ACTH-secreting tumors and their metastases, and especially for occult tumors.
  • A large variety of lesions in and around the pituitary region express somatostatin receptors and, therefore, can be visualized by 111In-pentetreotide scintigraphy.
  • [MeSH-minor] Carcinoid Tumor / radionuclide imaging. Gastrointestinal Neoplasms / radionuclide imaging. Humans. Indium Radioisotopes. Paraganglioma / radionuclide imaging. Pheochromocytoma / radionuclide imaging. Pituitary Neoplasms / radionuclide imaging. Receptors, Somatostatin / analysis

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  • (PMID = 16625862.001).
  • [ISSN] 0391-4097
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Indium Radioisotopes; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 0 / somatostatin receptor 5; 51110-01-1 / Somatostatin; G083B71P98 / pentetreotide
  • [Number-of-references] 49
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23. Jiang ZQ, Gui SB, Zhang YZ: Differential gene expression by fiber-optic beadarray and pathway in adrenocorticotrophin-secreting pituitary adenomas. Chin Med J (Engl); 2010 Dec;123(23):3455-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential gene expression by fiber-optic beadarray and pathway in adrenocorticotrophin-secreting pituitary adenomas.
  • BACKGROUND: Adrenocorticotrophin (ACTH)-secreting pituitary adenomas account for approximately 7% - 14% of all pituitary adenomas, but its pathogenesis is still enigmatic.
  • This study aimed to explore mechanisms underlying the pathogenesis of ACTH-secreting pituitary adenomas.
  • METHODS: We used fiber-optic beadarray to examine gene expression in three ACTH-secreting adenomas compared with three normal pituitaries.
  • Four differentially expressed genes from the three ACTH-secreting adenomas and three normal pituitaries were chosen randomly for validation by reverse transcriptase-real time quantitative polymerase chain reaction (RT-qPCR).
  • Bioinformatic and pathway analysis showed that the genes HIGD1B, EPS8, HPGD, DAPK2, and IGFBP3 and the transforming growth factor (TGF)-β signaling pathway and extracellular matrix (ECM)-receptor interaction pathway may play important roles in tumorigenesis and progression of ACTH-secreting pituitary adenomas.
  • CONCLUSIONS: Our data suggest that numerous aberrantly expressed genes and several pathways are involved in the pathogenesis of ACTH-secreting pituitary adenomas.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / etiology. Adenoma / etiology. Gene Expression Profiling. Oligonucleotide Array Sequence Analysis / methods. Signal Transduction / physiology
  • [MeSH-minor] Adult. Disease Progression. Expressed Sequence Tags. Extracellular Matrix Proteins / physiology. Female. Fiber Optic Technology. Humans. Male. Middle Aged. Real-Time Polymerase Chain Reaction. Reverse Transcriptase Polymerase Chain Reaction. Transforming Growth Factor alpha / physiology

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  • (PMID = 22166531.001).
  • [ISSN] 0366-6999
  • [Journal-full-title] Chinese medical journal
  • [ISO-abbreviation] Chin. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Extracellular Matrix Proteins; 0 / Transforming Growth Factor alpha
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24. Sahdev A, Reznek RH, Evanson J, Grossman AB: Imaging in Cushing's syndrome. Arq Bras Endocrinol Metabol; 2007 Nov;51(8):1319-28
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  • [Title] Imaging in Cushing's syndrome.
  • Once the diagnosis of Cushing's syndrome (CS) has been established, the main step is to differentiate between ACTH dependent and independent disease.
  • In adults, 80% of CS is due to ACTH-dependent causes and 20% due to adrenal causes.
  • ACTH-secreting neoplasms cause ACTH-dependent CS.
  • These are usually anterior pituitary microadenomas, which result in the classic Cushing's disease.
  • Non-pituitary ectopic sources of ACTH, such as a small-cell lung carcinoma or carcinoid tumours, are the source of the remainder of ACTH-dependent disease.
  • Imaging is essential for determining the source of ACTH in ectopic ACTH production, locating the pituitary tumours and distinguishing adrenal adenomas, carcinomas and hyperplasias.
  • In our chapter we review the adrenal appearances in ACTH-dependent and ACTH-independent CS.
  • We also include a discussion on the use of MRI and CT for the detection and management of pituitary ACTH secreting adenomas.
  • CT of the chest, abdomen and pelvis with intravenous injection of contrast medium is the most sensitive imaging modality for the identification of the ectopic ACTH source and detecting adrenal pathology.
  • MRI is used for characterising adrenal adenomas, problem solving in difficult cases and for detecting ACTH-secreting pituitary adenomas.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / diagnosis. Cushing Syndrome / diagnosis. Pituitary Gland / pathology. Pituitary Neoplasms / diagnosis
  • [MeSH-minor] ACTH Syndrome, Ectopic / diagnosis. Adenoma / diagnosis. Adenoma / radiography. Adrenal Gland Neoplasms / diagnosis. Adrenal Gland Neoplasms / radiography. Carcinoma / diagnosis. Carcinoma / radiography. Humans. Hyperplasia / diagnosis. Hyperplasia / radiography. Lung Neoplasms / diagnosis. Lung Neoplasms / secretion. Magnetic Resonance Imaging. Tomography, X-Ray Computed

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  • (PMID = 18209870.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Brazil
  • [Number-of-references] 36
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25. Mezosi E, Nemes O: [Treatment of pituitary adenomas]. Orv Hetil; 2009 Sep 27;150(39):1803-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Treatment of pituitary adenomas].
  • According to epidemiological studies, the prevalence of pituitary adenomas is 16.5% and the majority of them are "incidentalomas".
  • The symptoms of pituitary disorders are often non-specific; disturbances of pituitary function, compression symptoms, hypophysis apoplexy or accidental findings may help the diagnosis.
  • The hormonal evaluation of pituitary adenomas is different from the algorithm used in the disorders of peripheral endocrine organs.
  • The first-line therapy of prolactinomas are the dopamine agonists, and the aims of the treatment are to normalize the prolactin level, restore fertility in child-bearing age, decrease tumor mass, save or improve the residual pituitary function and inhibit the relapse of the disease.
  • In case of tumors with good therapeutic response, medical therapy can be withdrawn after 3-5 years; hyperprolactinemia will not recur in 2/3 of these patients.
  • Neurosurgery is the primary therapy of GH-, ACTH-, TSH-producing and inactive adenomas.
  • The medical therapy of Cushing's disease is still based on the inhibition of steroid production.
  • The rare TSH-producing tumor can respond to both dopamine agonist and somatostatin analog therapy.
  • Further studies are needed to elucidate the exact role of radiosurgery and fractionated stereotaxic irradiation in the treatment of pituitary tumors.
  • [MeSH-major] Adenoma / therapy. Pituitary Hormones / blood. Pituitary Neoplasms / therapy
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / therapy. Acromegaly / drug therapy. Acromegaly / etiology. Adrenocorticotropic Hormone / blood. Aminoquinolines / therapeutic use. Bromocriptine / therapeutic use. Cushing Syndrome / drug therapy. Cushing Syndrome / etiology. Dopamine Agonists / therapeutic use. Female. Growth Hormone-Secreting Pituitary Adenoma / therapy. Human Growth Hormone / analogs & derivatives. Human Growth Hormone / blood. Human Growth Hormone / therapeutic use. Humans. Hypophysectomy. Incidental Findings. Male. Pregnancy. Pregnancy Complications, Neoplastic / therapy. Prolactinoma / therapy. Radiosurgery. Receptors, Somatotropin / antagonists & inhibitors. Somatostatin / analogs & derivatives. Somatostatin / therapeutic use. Thyrotropin / blood

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  • (PMID = 19758960.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / Dopamine Agonists; 0 / Pituitary Hormones; 0 / Receptors, Somatotropin; 0 / pegvisomant; 12629-01-5 / Human Growth Hormone; 3A64E3G5ZO / Bromocriptine; 51110-01-1 / Somatostatin; 80Q9QWN15M / quinagolide; 9002-60-2 / Adrenocorticotropic Hormone; 9002-71-5 / Thyrotropin; 98H1T17066 / pasireotide
  • [Number-of-references] 28
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26. Vassiliadi D, Tsagarakis S: Unusual causes of Cushing's syndrome. Arq Bras Endocrinol Metabol; 2007 Nov;51(8):1245-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Unusual causes of Cushing's syndrome.
  • Although in the majority of the patients with Cushing's syndrome (CS), hypercortisolism is due to ACTH hypersecretion by a pituitary tumour or to ectopic ACTH secretion from an extrapituitary neoplastic lesion or to autonomous cortisol secretion by an adrenal tumour, in occasional patients a much rarer entity may be the cause of the syndrome.
  • The following unusual forms of CS were identified: (i) ACTH hyperesecretion due to ectopic corticotroph adenomas in the parasellar region or the neurohypophysis, or as part of double adenomas, or gangliocytomas;.
  • (ii) ACTH hypersecretion due to ectopic CRH or CRH-like peptide secretion by various neoplasms;.
  • (iii) ACTH-independent cortisol hypersecretion from ectopic or bilateral adrenal adenomas;.
  • Such unusual presentations of CS illustrate why Cushing's syndrome represents one of the most puzzling endocrine syndromes.
  • [MeSH-minor] ACTH Syndrome, Ectopic / complications. Adrenal Gland Neoplasms / complications. Female. Glucocorticoids / adverse effects. Humans. Liver Neoplasms / complications. Megestrol Acetate / adverse effects. Ovarian Neoplasms / complications. Pituitary Neoplasms / complications. Ritonavir / adverse effects

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  • (PMID = 18209862.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Glucocorticoids; O3J8G9O825 / Ritonavir; TJ2M0FR8ES / Megestrol Acetate
  • [Number-of-references] 58
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27. Matsuno A: [Recent trends in the pathophysiology and treatment of pituitary adenomas]. Brain Nerve; 2009 Aug;61(8):957-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Recent trends in the pathophysiology and treatment of pituitary adenomas].
  • Recent molecular pathological investigations have elucidated the cytodifferentiation of pituitary cells and identified several transcriptional factors that regulate this cytodifferentiation of pituitary cells.
  • The patterns of cytodifferentiation are closely related to the pathogenesis of pituitary adenomas.
  • Meanwhile, the role of hypothalamic hormones in the development of pituitary adenomas has recently attracted the attention of investigators.
  • The expression of growth hormone-releasing hormone and corticotrophin releasing hormone in corticotroph adenomas have been demonstrated in somatotroph adenomas and corticotropin adenomas, respectively.
  • This finding indicates that the endogenous expression of hypothalamic hormones and their receptors in human pituitary adenoma cells has ample significance in the autocrine or paracrine regulation of pituitary hormone production and tumor extension induced by hypothalamic hormones produced by adenoma cells.
  • The recent progress in surgical techniques for treatment of pituitary adenomas has provided several alternatives: transsphenoidal surgery vs. transcranial surgery, sublabial approach vs. endonasal approach, and microsurgery vs. endoscopic surgery.
  • There have also been developments in the medical treatment of pituitary adenomas.
  • The frequently used dopamine agonist, cabergoline, is very effective for treating prolactin-producing adenoma.
  • Long-acting octreotide and pegvisomant are now available for the treatment of growth hormone producing adenoma.
  • Cabergoline is also used for growth hormone producing adenoma.
  • Temozolomide has recently been used for atypical adenomas or pituitary carcinomas.
  • Adult growth hormone deficiency sometimes occurs in postoperative patients with pituitary adenomas.
  • [MeSH-major] Adenoma / etiology. Adenoma / therapy. Pituitary Neoplasms / etiology. Pituitary Neoplasms / therapy
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Corticotropin-Releasing Hormone. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use. Ergolines / therapeutic use. Growth Hormone-Releasing Hormone. Human Growth Hormone / analogs & derivatives. Human Growth Hormone / therapeutic use. Humans. Hypothalamic Hormones. Incidental Findings. Neurosurgical Procedures / methods. Neurosurgical Procedures / trends. Octreotide / therapeutic use. Prolactinoma. Receptors, Neuropeptide. Receptors, Pituitary Hormone-Regulating Hormone

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  • (PMID = 19697885.001).
  • [ISSN] 1881-6096
  • [Journal-full-title] Brain and nerve = Shinkei kenkyū no shinpo
  • [ISO-abbreviation] Brain Nerve
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ergolines; 0 / Hypothalamic Hormones; 0 / Receptors, Neuropeptide; 0 / Receptors, Pituitary Hormone-Regulating Hormone; 0 / pegvisomant; 0 / somatotropin releasing hormone receptor; 12629-01-5 / Human Growth Hormone; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; 9015-71-8 / Corticotropin-Releasing Hormone; 9034-39-3 / Growth Hormone-Releasing Hormone; LL60K9J05T / cabergoline; RWM8CCW8GP / Octreotide
  • [Number-of-references] 32
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28. Penezić Z, Zarković M, Vujović S, Ivović M, Beleslin B, Ciric J, Drezgić M: [The value of corticotropin-releasing hormone (CRH) test for differential diagnosis of Cushing's syndrome]. Srp Arh Celok Lek; 2007 Jan-Feb;135(1-2):31-7
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  • [Title] [The value of corticotropin-releasing hormone (CRH) test for differential diagnosis of Cushing's syndrome].
  • INTRODUCTION: Diagnosis and differential diagnosis of Cushing's syndrome (CS) remain considerable challenge in endocrinology.
  • Following the CRH administration, the majority of patients with ACTH secreting pituitary adenoma show a significant rise of plasma cortisol and ACTH, whereas those with ectopic ACTH secretion characteristically do not.
  • OBJECTIVE: The aim of our study was to assess the value of CRF test for differential diagnosis of CS using the ROC (receiver operating characteristic) curve method.
  • ACTH secreting pituitary adenoma was found in 18, ectopic ACTH secretion in 3 and cortisol secreting adrenal adenoma in 9 of all patients with CS.
  • Cortisol and ACTH were determined -15.0, 15, 30, 45, 60, 90 and 120 min. after i.v. administration of 100 microg of ovine CRH.
  • Cortisol and ACTH were determined by commercial RIA.
  • Due to small number, the patients with ectopic ACTH secretion were excluded from test evaluation by ROC curve method.
  • Consequently, basal ACTH was (100.9 +/- 85.0 vs. 138.0 +/- 123.7 vs. 4.8 +/- 4.3 pg/mL) and maximal stimulated ACTH (203.8 +/- 160.1 vs. 288.0 +/- 189.5 vs. 7.4 +/- 9.2 pg/mL).
  • For ACTH, determination area under ROC curve was 0.637 +/- 0.142 (CI 95% 0.359-0.916).
  • For ACTH increase cut-off level of 30%, test sensitivity was 70%, with specificity of 57%.
  • CONCLUSION: Determination of cortisol and ACTH levels in CRH test remains reliable tool in differential diagnosis of Cushing's syndrome.
  • [MeSH-major] Corticotropin-Releasing Hormone. Cushing Syndrome / diagnosis
  • [MeSH-minor] ACTH Syndrome, Ectopic / diagnosis. ACTH-Secreting Pituitary Adenoma / diagnosis. Adenoma / diagnosis. Adrenocorticotropic Hormone / blood. Adult. Diagnosis, Differential. Female. Humans. Hydrocortisone / blood. Male. ROC Curve. Sensitivity and Specificity

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  • (PMID = 17503565.001).
  • [ISSN] 0370-8179
  • [Journal-full-title] Srpski arhiv za celokupno lekarstvo
  • [ISO-abbreviation] Srp Arh Celok Lek
  • [Language] srp
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Serbia and Montenegro
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone; WI4X0X7BPJ / Hydrocortisone
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29. Cho HY, Cho SW, Kim SW, Shin CS, Park KS, Kim SY: Silent corticotroph adenomas have unique recurrence characteristics compared with other nonfunctioning pituitary adenomas. Clin Endocrinol (Oxf); 2010 May;72(5):648-53
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  • [Title] Silent corticotroph adenomas have unique recurrence characteristics compared with other nonfunctioning pituitary adenomas.
  • OBJECTIVE: The prevalence of silent corticotroph adenomas (SCAs) is not rare among nonfunctioning pituitary adenomas (NFPAs); however, it is unknown whether the clinical significance of SCAs differs from that of NFPAs without ACTH immunoreactivity (non-SCAs).
  • MEASUREMENTS: We analysed whether clinical manifestations at diagnosis, postoperative recurrence rate and recurrence characteristics differed between SCA and non-SCA patients.
  • The mean age at the time of diagnosis was 44 years (range, 13-67 years) in the SCA group and 50 years (18-79 years) in the non-SCA group (P = 0.026), with respective follow-up periods of 5.2 (range, 1.0-16.0 years) and 4.2 years (0.5-16.1 years) (P = 0.255).
  • [MeSH-major] Adenoma / pathology. Adrenocorticotropic Hormone / analysis. Neoplasm Recurrence, Local. Pituitary Neoplasms / pathology

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  • (PMID = 19650787.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
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30. Fernando MA, Heaney AP: Alpha1-adrenergic receptor antagonists: novel therapy for pituitary adenomas. Mol Endocrinol; 2005 Dec;19(12):3085-96
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  • [Title] Alpha1-adrenergic receptor antagonists: novel therapy for pituitary adenomas.
  • Pituitary tumors are common and cause considerable morbidity due to local invasion and altered hormone secretion.
  • Doxazosin (dox), a selective alpha(1)-adrenergic receptor antagonist, used to treat hypertension, also inhibits prostate cancer cell proliferation.
  • We examined the effects of dox on murine and human pituitary tumor cell proliferation in vitro and in vivo. dox treatment inhibited proliferation of murine pituitary tumor cells, induced G(0)-G(1) cell cycle arrest, and reduced phosphorylated retinoblastoma levels.
  • In addition, increased annexin-fluorescein isothiocyanate immunoreactivity and cleaved caspase-3 levels, in keeping with dox-mediated apoptosis, were observed in the human and murine pituitary tumor cells, and dox administration to mice, harboring corticotroph tumors, decreased tumor growth and reduced plasma ACTH levels. dox-mediated antiproliferative and proapoptotic actions were not confined to alpha-adrenergic receptor-expressing pituitary tumor cells and were unaffected by cotreatment with the alpha-adrenergic receptor blocker, phenoxybenzamine. dox treatment led to reduced phosphorylated inhibitory kappaB (IkappaB)-alpha expression, and nuclear factor-kappaB transcription and decreased basal and TNFalpha-induced proopiomelanocortin transcriptional activation.
  • These results demonstrate that the selective alpha(1)-adrenergic receptor antagonist dox inhibits pituitary tumor cell growth in vitro and in vivo by mechanisms that are in part independent of its alpha-adrenergic receptor-blocking actions and involve down-regulation of nuclear factor-kappaB signaling. dox is proposed as a possible novel medical therapy for pituitary tumors.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / drug therapy. Adenoma / drug therapy. Adrenergic alpha-1 Receptor Antagonists. Adrenergic alpha-Antagonists / therapeutic use. Antineoplastic Agents / therapeutic use. Doxazosin / therapeutic use
  • [MeSH-minor] Adrenocorticotropic Hormone / blood. Animals. Apoptosis. Caspase 3. Caspases / metabolism. Cell Cycle / drug effects. Cell Proliferation / drug effects. Humans. I-kappa B Proteins / metabolism. Mice. Mice, Nude. NF-kappa B / metabolism. Neoplasm Transplantation. Pro-Opiomelanocortin / genetics. Receptors, Adrenergic, alpha-1 / genetics. Receptors, Adrenergic, alpha-1 / metabolism. Transcriptional Activation. Tumor Cells, Cultured. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 16020484.001).
  • [ISSN] 0888-8809
  • [Journal-full-title] Molecular endocrinology (Baltimore, Md.)
  • [ISO-abbreviation] Mol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenergic alpha-1 Receptor Antagonists; 0 / Adrenergic alpha-Antagonists; 0 / Antineoplastic Agents; 0 / I-kappa B Proteins; 0 / NF-kappa B; 0 / Receptors, Adrenergic, alpha-1; 0 / Tumor Necrosis Factor-alpha; 139874-52-5 / NF-kappaB inhibitor alpha; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; NW1291F1W8 / Doxazosin
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31. De Menis E, Roncaroli F, Calvari V, Chiarini V, Pauletto P, Camerino G, Cremonini N: Corticotroph adenoma of the pituitary in a patient with X-linked adrenal hypoplasia congenita due to a novel mutation of the DAX-1 gene. Eur J Endocrinol; 2005 Aug;153(2):211-5
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  • [Title] Corticotroph adenoma of the pituitary in a patient with X-linked adrenal hypoplasia congenita due to a novel mutation of the DAX-1 gene.
  • We report the occurrence of an ACTH-secreting adenoma in a patient with X-linked congenital adrenal hypoplasia.
  • DESIGN AND METHODS: Detailed clinical, radiological and pathological investigation of the pituitary adenoma.
  • ACTH was 24 980 pg/ml and nuclear magnetic resonance disclosed a huge pituitary adenoma.
  • Three transsphenoidal operations and radiotherapy were necessary to remove the tumor mass and control ACTH secretion.
  • Histologically, the adenoma was composed of chromophobic and basophilic neoplastic cells with positive immunostaining for ACTH.
  • CONCLUSIONS: This case suggests that in adrenal hypoplasia congenita the development of a pituitary adenoma should be considered when a sudden rise of ACTH occurs despite adequate steroid substitution.
  • [MeSH-major] Adenoma / complications. Adrenal Insufficiency / complications. Adrenal Insufficiency / genetics. DNA-Binding Proteins / genetics. Pituitary Neoplasms / complications. Receptors, Retinoic Acid / genetics. Repressor Proteins / genetics
  • [MeSH-minor] Adrenocorticotropic Hormone / metabolism. Adult. Chromosomes, Human, X. DAX-1 Orphan Nuclear Receptor. Family Health. Female. Frameshift Mutation. Humans. Magnetic Resonance Imaging. Male. Pituitary ACTH Hypersecretion / complications. Pituitary ACTH Hypersecretion / metabolism. Pituitary ACTH Hypersecretion / pathology

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  • (PMID = 16061826.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] eng
  • [Grant] Italy / Telethon / / B.38
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DAX-1 Orphan Nuclear Receptor; 0 / DNA-Binding Proteins; 0 / NR0B1 protein, human; 0 / Receptors, Retinoic Acid; 0 / Repressor Proteins; 9002-60-2 / Adrenocorticotropic Hormone
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32. Brown RL, Wollman R, Weiss RE: Transformation of a pituitary macroadenoma into to a corticotropin-secreting carcinoma over 16 years. Endocr Pract; 2007 Sep;13(5):463-71
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  • [Title] Transformation of a pituitary macroadenoma into to a corticotropin-secreting carcinoma over 16 years.
  • OBJECTIVE: To describe a case of a pituitary macroadenoma that differentiated into a corticotropin (ACTH)-secreting carcinoma with metastasis to the thigh.
  • METHODS: We present a case report with a 16-year follow-up that includes anatomic and endocrine documentation of the history of an ACTH-secreting carcinoma.
  • Magnetic resonance imaging revealed a locally invasive 3-cm macroadenoma.
  • The patient underwent surgical debulking followed by a course of radiation directed to the pituitary.
  • Results from retrospective immunohistochemical staining with antibodies against ACTH, prolactin, and MIB-1 were negative.
  • Postoperatively, she could not be weaned from exogenous steroids without developing symptoms of adrenal insufficiency.
  • In 1995, she developed left facial palsy and diplopia caused by tumor growth.
  • The patient's clinical status continued to deteriorate because of local mass effect from tumor growth and uncontrolled hypercortisolism.
  • The patient remained debilitated in a long-term care facility for 2 years when she was found to have a mass on her left hip.
  • Biopsy results of the obturator muscle revealed metastatic tumor of neuroendocrine origin with strong reactivity to ACTH antibodies and MIB-1 labeling in 8% of tumor cell nuclei.
  • CONCLUSION: A pituitary tumor can transform into an ACTH-secreting carcinoma in an indolent manner.
  • Patients with invasive pituitary adenomas require long-term surveillance to monitor for differentiation into pituitary carcinoma.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / pathology. ACTH-Secreting Pituitary Adenoma / secretion. Adenoma / pathology. Adenoma / secretion. Adrenocorticotropic Hormone / secretion
  • [MeSH-minor] Adult. Biopsy. Disease Progression. Female. Humans. Hypophysectomy. Magnetic Resonance Imaging. Muscle, Skeletal / pathology. Radiosurgery. Tomography, X-Ray Computed

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  • (PMID = 17872347.001).
  • [ISSN] 1934-2403
  • [Journal-full-title] Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists
  • [ISO-abbreviation] Endocr Pract
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK07011; United States / NCRR NIH HHS / RR / RR00055; United States / NCRR NIH HHS / RR / RR18372
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
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33. Salgado LR, Machado MC, Cukiert A, Liberman B, Kanamura CT, Alves VA: Cushing's disease arising from a clinically nonfunctioning pituitary adenoma. Endocr Pathol; 2006;17(2):191-9
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  • [Title] Cushing's disease arising from a clinically nonfunctioning pituitary adenoma.
  • A 49-yr-old woman with a large pituitary tumor leading to visual loss and galactorrhea- amenorrhea was submitted to transcranial pituitary surgery, when a clinically nonfunctioning pituitary adenoma was partially removed.
  • Histopathology and immunohistochemistry confirmed the diagnosis of "non-secreting atypical adenoma."
  • Two years later, she presented high free urinary cortisol levels and a positive ACTH response to desmopressin testing on dexametasone 2 mg overnight.
  • A pituitary biopsy confirmed aggressive growth as well as positive immunoreactivity for ACTH, p53, Ki-67, and c-erb-B2.
  • The overall clinical, laboratory, and pathological data suggest a transition from a clinically nonfunctioning to a hypersecreting ACTH-producing tumor.
  • Putative mechanisms of tumor transformation and the possibility of a silent corticotropinoma evolving into clinical Cushing s syndrome are discussed.
  • [MeSH-major] Adenoma / complications. Adenoma / pathology. Pituitary ACTH Hypersecretion / etiology. Pituitary Neoplasms / complications. Pituitary Neoplasms / pathology

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  • [Cites] Pituitary. 2000 Oct;3(2):117-22 [11141695.001]
  • [Cites] Neurosurgery. 1996 Apr;38(4):765-70; discussion 770-1 [8692397.001]
  • [Cites] Clin Endocrinol (Oxf). 1997 May;46(5):599-606 [9231056.001]
  • [Cites] Endocr Pathol. 1996 Spring;7(1):21-35 [12114677.001]
  • [Cites] J Neurosurg. 2004 Nov;101(5):874-7 [15540932.001]
  • [Cites] Aust N Z J Med. 1987 Apr;17(2):249-51 [3039955.001]
  • [Cites] Arch Intern Med. 1983 May;143(5):1040-2 [6089681.001]
  • [Cites] J Endocrinol Invest. 1997 Apr;20(4):240-4 [9211134.001]
  • [Cites] Clin Endocrinol (Oxf). 1985 Feb;22(2):147-53 [2985300.001]
  • [Cites] Neurosurgery. 1996 Jan;38(1):99-106; discussion 106-7 [8747957.001]
  • [Cites] Endocr J. 2002 Jun;49(3):285-92 [12201210.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Nov;79(5):1513-6 [7962351.001]
  • [Cites] Front Horm Res. 2004;32:205-16 [15281348.001]
  • [Cites] Br J Neurosurg. 2005 Feb;19(1):38-42 [16147581.001]
  • [Cites] J Clin Endocrinol Metab. 1998 May;83(5):1619-23 [9589666.001]
  • [Cites] Endocrinol Metab Clin North Am. 1989 Jun;18(2):339-58 [2663478.001]
  • [Cites] Clin Endocrinol (Oxf). 1994 Nov;41(5):661-6 [7828356.001]
  • [Cites] Pituitary. 2002;5(4):221-3 [14558669.001]
  • [Cites] J Clin Endocrinol Metab. 1993 May;76(5):1089-94 [8496297.001]
  • [Cites] J Clin Endocrinol Metab. 1979 Jul;49(1):23-9 [221528.001]
  • [Cites] Endocr Pathol. 1996 Summer;7(2):145-150 [12114642.001]
  • (PMID = 17159252.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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34. Barlier A, Vanbellinghen JF, Daly AF, Silvy M, Jaffrain-Rea ML, Trouillas J, Tamagno G, Cazabat L, Bours V, Brue T, Enjalbert A, Beckers A: Mutations in the aryl hydrocarbon receptor interacting protein gene are not highly prevalent among subjects with sporadic pituitary adenomas. J Clin Endocrinol Metab; 2007 May;92(5):1952-5
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  • [Title] Mutations in the aryl hydrocarbon receptor interacting protein gene are not highly prevalent among subjects with sporadic pituitary adenomas.
  • CONTEXT: Limited screening suggests that three germline mutations in the aryl hydrocarbon receptor interacting protein (AIP) gene are not involved in sporadic pituitary tumorigenesis.
  • Multiple novel mutations of this gene have since been identified in familial isolated pituitary adenoma cohorts.
  • OBJECTIVE: The objective of the study was to undertake full AIP coding sequence screening to assess for the presence of germline and somatic mutations in European Union subjects with sporadic pituitary tumors.
  • Multiplex ligation-dependent probe amplification was used to screen separate sporadic pituitary tumor tissue samples for discrete and extensive deletions or mutations of the AIP gene.
  • RESULTS: In 107 patients [prolactinomas (n =49), nonfunctioning tumors (n = 29), somatotropinomas (n = 26), ACTH-secreting tumors (n = 2), TSH-secreting tumors (n = 1)], no germline mutations of AIP were demonstrated.
  • Among a group of 41 tumor samples from other subjects, a novel AIP mutation (R22X) was found in one sample in which the corresponding allele was deleted; follow-up screening of the patient demonstrated a germline R22X AIP mutation.
  • CONCLUSIONS: AIP mutations do not appear to play a prominent role in sporadic pituitary tumorigenesis in this population of European subjects.
  • [MeSH-major] Adenoma / genetics. Mutation / genetics. Pituitary Neoplasms / genetics. Proteins / genetics
  • [MeSH-minor] Adult. DNA, Neoplasm / genetics. Female. Gene Frequency. Genotype. Humans. Intracellular Signaling Peptides and Proteins. Male. Middle Aged. Multiple Endocrine Neoplasia Type 1 / genetics. Polymorphism, Genetic / genetics

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  • [CommentIn] J Clin Endocrinol Metab. 2007 May;92(5):1617-9 [17483376.001]
  • (PMID = 17299063.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Intracellular Signaling Peptides and Proteins; 0 / Proteins; 0 / aryl hydrocarbon receptor-interacting protein
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35. Eljamel MS, Leese G, Moseley H: Intraoperative optical identification of pituitary adenomas. J Neurooncol; 2009 May;92(3):417-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Intraoperative optical identification of pituitary adenomas.
  • INTRODUCTION: The main goals of transsphenoidal pituitary surgery are total removal of pituitary adenomas (PAs) and preservation of normal pituitary functions.
  • Achieving these goals is dependent upon the precise localisation of PAs during surgery, particularly secreting microadenomas.
  • After the dura of the floor of the sella was incised a laser probe was inserted into the pituitary gland to identify the ALA-induced protoporphyrin IX spectroscopy at 632 nm, using an optical biopsy system (OBS).
  • Once the adenoma was identified by the OBS it was exposed and examined by the PD system to detect fluorescence.
  • PATIENTS: Thirty consecutive patients were studied: 14 were non-functioning macroadenomas (NFA), 12 were secreting PAs and 4 pituitary cysts.
  • The secreting PAs were GH (2), ACTH (3), prolactin (2) and gonadotrophins (5).
  • Six were microadenomas (3 ACTH, 1 GH, 2 prolactin) and 20 were macroadenomas, of which 12 were invading macroadenomas.
  • CONCLUSION: Intraoperative optical identification of pituitary adenomas is a feasible and reliable way to localize pituitary adenomas during transsphenoidal surgery and it may lead to improved cure rate and preservation of normal pituitary functions.
  • [MeSH-major] Adenoma / pathology. Diagnostic Imaging / methods. Pituitary Neoplasms / pathology

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  • [Cites] N Engl J Med. 1991 Sep 26;325(13):897-905 [1652686.001]
  • [Cites] Neurosurgery. 2001 Oct;49(4):857-62; discussion 862-3 [11564246.001]
  • [Cites] Clin Endocrinol (Oxf). 1996 Aug;45(2):147-56 [8881446.001]
  • [Cites] Radiology. 1992 Oct;185(1):143-7 [1523298.001]
  • [Cites] Clin Endocrinol (Oxf). 1995 Nov;43(5):517-22 [8548933.001]
  • [Cites] J Neurosurg. 1986 May;64(5):713-9 [3701419.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Sep;86(9):4072-7 [11549628.001]
  • [Cites] Surg Neurol. 2000 Mar;53(3):211-9 [10773251.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Sep;84(9):3401-2 [10487721.001]
  • [Cites] Lancet Oncol. 2006 May;7(5):392-401 [16648043.001]
  • [Cites] Acta Neurochir Suppl (Wien). 1991;53:72-6 [1803889.001]
  • [Cites] Clin Endocrinol (Oxf). 1988 Mar;28(3):289-95 [2844450.001]
  • [Cites] Br J Neurosurg. 1999 Aug;13(4):349-51 [10616559.001]
  • [Cites] Ann Intern Med. 1988 Sep 15;109(6):487-93 [2843068.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Sep;90(9):5134-40 [15941871.001]
  • [Cites] Endocr Pract. 1998 Nov-Dec;4(6):365-7 [15251709.001]
  • [Cites] Pituitary. 1999 Aug;2(2):117-22 [11081161.001]
  • [Cites] Technol Cancer Res Treat. 2003 Aug;2(4):303-9 [12892512.001]
  • [Cites] Radiother Oncol. 1999 Sep;52(3):233-7 [10580869.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Feb;84(2):487-92 [10022405.001]
  • [Cites] Neuroradiology. 1998 Oct;40(10 ):651-5 [9833894.001]
  • [Cites] J Endocrinol Invest. 2000 Sep;23(8):542-4 [11021772.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Aug;89(8):3752-63 [15292301.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Jul;83(7):2291-5 [9661597.001]
  • [Cites] J Neurosurg. 1986 Dec;65(6):733-44 [3095506.001]
  • [Cites] J Neurosurg. 1998 Dec;89(6):927-32 [9833817.001]
  • [Cites] Neurol Neurochir Pol. 2004 May-Jun;38(3):201-7 [15354233.001]
  • [Cites] J Neurosurg. 2002 Feb;96(2):195-208 [11838791.001]
  • [Cites] AJNR Am J Neuroradiol. 2000 Apr;21(4):690-6 [10782779.001]
  • [Cites] Neurosurgery. 1995 Sep;37(3):541-5; discussion 545-6 [7501126.001]
  • (PMID = 19357967.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Photosensitizing Agents; 88755TAZ87 / Aminolevulinic Acid
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36. van der Hoek J, Lamberts SW, Hofland LJ: The somatostatin receptor subtype 5 in neuroendocrine tumours. Expert Opin Investig Drugs; 2010 Mar;19(3):385-99
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • AREAS COVERED IN THIS REVIEW: The scope of this review is primarily focused upon recent insights in sst(5)-receptor physiology, novel sst(5)-targeted treatment options predominantly directed towards pituitary adenomas, and gastroenteropancreatic neuroendocrine tumours.
  • WHAT THE READER WILL GAIN: An understanding of the potential that novel sst(5)-targeted SRIF analogues might have in the medical treatment of Cushing's disease and acromegaly, as demonstrated by translational research, based on pathophysiological data combined with results from clinical trials.
  • Finally, absence of sst(5) in corticotroph adenomas could be related to tumour aggressiveness in Cushing's disease.
  • [MeSH-minor] Adenoma / drug therapy. Adenoma / physiopathology. Animals. Drug Design. Gastrointestinal Neoplasms / drug therapy. Gastrointestinal Neoplasms / physiopathology. Humans. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / physiopathology. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / physiopathology

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  • (PMID = 20151855.001).
  • [ISSN] 1744-7658
  • [Journal-full-title] Expert opinion on investigational drugs
  • [ISO-abbreviation] Expert Opin Investig Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Somatostatin; 0 / somatostatin receptor 5
  • [Number-of-references] 101
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37. Aghi MK: Management of recurrent and refractory Cushing disease. Nat Clin Pract Endocrinol Metab; 2008 Oct;4(10):560-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Management of recurrent and refractory Cushing disease.
  • Cushing disease is most frequently caused by pituitary adenomas that secrete adrenocorticotrophic hormone.
  • More challenging for neurosurgeons and endocrinologists, however, is management of the remaining patients whose Cushing disease is refractory to initial transsphenoidal surgery or recurs after initial remission.
  • Here, we review the treatment options and latest surgical, medical, and radiosurgical advances for patients who have persistent or recurrent Cushing disease after transsphenoidal surgery.
  • [MeSH-major] Pituitary ACTH Hypersecretion / therapy
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / complications. ACTH-Secreting Pituitary Adenoma / surgery. Adrenalectomy. Humans. Hypophysectomy / methods. Ketoconazole / therapeutic use. Models, Biological. Neoplasm Recurrence, Local / surgery. Pituitary Neoplasms / complications. Pituitary Neoplasms / surgery. Radiosurgery / methods. Recurrence. Sphenoid Bone / surgery. Treatment Failure

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  • (PMID = 18711406.001).
  • [ISSN] 1745-8374
  • [Journal-full-title] Nature clinical practice. Endocrinology & metabolism
  • [ISO-abbreviation] Nat Clin Pract Endocrinol Metab
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] R9400W927I / Ketoconazole
  • [Number-of-references] 54
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38. Krikorian A, Abdelmannan D, Selman WR, Arafah BM: Cushing disease: use of perioperative serum cortisol measurements in early determination of success following pituitary surgery. Neurosurg Focus; 2007;23(3):E6
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  • [Title] Cushing disease: use of perioperative serum cortisol measurements in early determination of success following pituitary surgery.
  • Despite many recent advances, management of cases of Cushing disease continues to be challenging.
  • After complete resection of ACTH-secreting adenomas, patients develop transient ACTH deficiency requiring glucocorticoid replacement for several months.
  • The current recommendation by many centers, including ours, for patients with ACTH-secreting adenomas is to withhold glucocorticoid therapy during and immediately after adenomectomy until there is clinical or biochemical evidence of ACTH deficiency.
  • A serum cortisol level of less than 2 microg/dl within the first 48 hours after adenomectomy is a reliable biochemical marker of ACTH deficiency and is associated with clinical remission of Cushing disease.
  • Optimal diagnosis and therapy for patients with Cushing disease require thorough and close coordination and involvement of all members of the management team.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / surgery. Hydrocortisone / blood. Pituitary ACTH Hypersecretion / blood. Pituitary ACTH Hypersecretion / surgery

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  • (PMID = 17961022.001).
  • [ISSN] 1092-0684
  • [Journal-full-title] Neurosurgical focus
  • [ISO-abbreviation] Neurosurg Focus
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucocorticoids; WI4X0X7BPJ / Hydrocortisone
  • [Number-of-references] 36
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39. Chacko G, Chacko AG, Lombardero M, Mani S, Seshadri MS, Kovacs K, Scheithauer BW: Clinicopathologic correlates of giant pituitary adenomas. J Clin Neurosci; 2009 May;16(5):660-5
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  • [Title] Clinicopathologic correlates of giant pituitary adenomas.
  • Giant adenomas comprise a clinical/therapeutic subset of pituitary adenomas that pose a surgical challenge.
  • The study population consisted of 28 patients who had giant pituitary adenomas, which are defined as tumors with a diameter greater than 5cm.
  • Clinically, five tumors (18%) were endocrinologically functional and 23 (82%) were not.
  • During surgery, one tumor was radically excised, four were subtotally excised, 12 were partially excised, and 11 were biopsied.
  • All of the tumors showed typical histological features of pituitary adenoma.
  • Of the 23 clinically non-functional adenomas, 18 were gonadotrophic tumors, four were null cell adenomas and one was a silent corticotroph adenoma.
  • The present study found giant adenomas to be invasive but slow growing, histologically benign and often gonadotrophic in subtype.
  • [MeSH-major] Adenoma / pathology. Adenoma / therapy. Pituitary Neoplasms / pathology. Pituitary Neoplasms / therapy
  • [MeSH-minor] Adolescent. Adrenocorticotropic Hormone / metabolism. Adult. Antigens, CD34 / metabolism. Female. Follow-Up Studies. Humans. Ki-67 Antigen / metabolism. Magnetic Resonance Imaging / methods. Male. Middle Aged. Neoplasm Invasiveness. Retrospective Studies. Treatment Outcome. Young Adult

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  • (PMID = 19285407.001).
  • [ISSN] 0967-5868
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Ki-67 Antigen; 9002-60-2 / Adrenocorticotropic Hormone
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40. Bernreuther C, Flitsch J, Lüdecke DK, Hagel C: A 61-year-old man with hyponatremia. Brain Pathol; 2008 Apr;18(2):283-7
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  • Endocrinologically, low levels for ADH, cortisol and testosterone as well as low-normal values for ACTH, LH and FSH were detected.
  • Cranial computed tomography and MRI scans revealed an intra- and suprasellar tumor of adenoma-like appearance with elevation of the optic chiasm.
  • After transsphenoidal resection of the tumor, no additional anterior lobe insufficiencies or diabetes insipidus occurred.
  • Histological examination revealed a tumor consisting of spindle-shaped cells of uniformly high cellularity with no evidence of hypocellular areas.
  • An intrasellar cellular schwannoma clinically and radiologically mimicking a non-secreting pituitary adenoma is uncommon.
  • However, rare entities like schwannomas, melanocytomas or pituicytomas have to be considered in addition to the more common tumors like pituitary adenomas and meningiomas.

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  • (PMID = 18363939.001).
  • [ISSN] 1015-6305
  • [Journal-full-title] Brain pathology (Zurich, Switzerland)
  • [ISO-abbreviation] Brain Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Switzerland
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41. Bademci G: Pitfalls in the management of Cushing's disease. J Clin Neurosci; 2007 May;14(5):401-8; discussion 409
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  • [Title] Pitfalls in the management of Cushing's disease.
  • Cushing's disease is caused by functional corticotroph adenomas of the pituitary gland, most commonly noninvasive microadenomas.
  • Transsphenoidal microsurgery is an effective means of control for patients with adrenocorticotrophic hormone-producing microadenomas.
  • The major causes of surgical failure in the treatment of Cushing's disease lies in inadequate preoperative evaluation, unsuccessful identification of the adenoma and inexperience of the surgeon.
  • For optimal results in this rare disease, endocrinological, radiological and surgical procedures should be co-ordinated in a specialized center.
  • [MeSH-major] Pituitary ACTH Hypersecretion / therapy. Treatment Failure

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  • (PMID = 17386367.001).
  • [ISSN] 0967-5868
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Scotland
  • [Number-of-references] 82
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42. Thodou E, Argyrakos T, Kontogeorgos G: Galectin-3 as a marker distinguishing functioning from silent corticotroph adenomas. Hormones (Athens); 2007 Jul-Sep;6(3):227-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Galectin-3 as a marker distinguishing functioning from silent corticotroph adenomas.
  • OBJECTIVE: Galectin-3 (Gal-3) belongs to the family of carbohydrate-binding proteins with high affinity for galactoside and is involved in many biological processes including cell growth and differentiation, cell adhesion, tumor progression, apoptosis and metastasis.
  • The aim of this study was to disclose differences in the expression of Gal-3 in silent and functioning corticotroph pituitary adenomas.
  • DESIGN: We examined 30 pituitary adenomas (19 functioning corticotroph, 11 silent corticotroph adenomas).
  • Two prolactinomas and 2 functioning somatotroph adenomas served as positive controls.
  • The independent variables t-test was used for comparison of the mean expression of Gal-3 in the two different corticotroph adenoma subgroups.
  • RESULTS: Eighteen of the functioning corticotroph adenomas (94.73%) were positive for Gal-3 with a cytoplasmic and focally membranous distribution; two cases also exhibited nuclear expression, whereas 9 of the silent corticotroph adenomas (81.81%) had zero or<1% expression of Gal-3 (p=0.001).
  • CONCLUSIONS: Gal-3 is highly expressed in functioning corticotroph adenomas of the pituitary gland, while silent adenomas exhibit very focal to null expression of Gal-3.
  • This observation can be used in the pathological diagnosis to separate functioning from silent corticotroph adenomas of the pituitary.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / diagnosis. Adenoma / diagnosis. Biomarkers, Tumor / metabolism. Galectin 3 / metabolism
  • [MeSH-minor] Humans. Immunohistochemistry. Pituitary Gland / metabolism

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  • (PMID = 17724007.001).
  • [ISSN] 1109-3099
  • [Journal-full-title] Hormones (Athens, Greece)
  • [ISO-abbreviation] Hormones (Athens)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Galectin 3
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43. Mounier C, Pasquet F, Trouillas J, Perrin G, Jouanneau E, Borson-Chazot F, Colle B: [Nelson's syndrome: course of aggressive pituitary corticotroph adenoma]. Ann Endocrinol (Paris); 2007 Feb;68(1):28-33
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  • [Title] [Nelson's syndrome: course of aggressive pituitary corticotroph adenoma].
  • [Transliterated title] Syndrome de Nelson: évolution d'un adénome hypophysaire corticotrope agressif.
  • Nelson's syndrome was defined in 1958 as the association of an expanding pituitary tumor with high ACTH secretion after bilateral adrenalectomy for Cushing's disease.
  • Pituitary MRI and ACTH measurements led to the definition of Nelson's syndrome as the proliferation of a corticotrophic microadenoma or an aggressive and highly proliferative tumor residue induced by the decreased glucocorticoid inhibition after bilateral adrenalectomy.
  • Now, the problem is not the definition of Nelson's syndrome but rather the identification of markers predictive of tumor growth.
  • Based on a typical case and a review of the literature, we point out some predictive markers of tumor growth after bilateral adrenalectomy: young age at diagnosis, presence of tumor residue on pituitary MRI before adrenalectomy, markers of tumor aggressiveness (Ki-67>3%, mitoses, nuclear PTTG) and increase of ACTH levels during the first months following adrenalectomy.
  • [MeSH-major] Adenoma / physiopathology. Nelson Syndrome / physiopathology. Pituitary Neoplasms / physiopathology
  • [MeSH-minor] Adrenocorticotropic Hormone / analysis. Adrenocorticotropic Hormone / secretion. Adult. Female. Humans. Magnetic Resonance Imaging. Pituitary Gland / pathology

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  • (PMID = 17306208.001).
  • [ISSN] 0003-4266
  • [Journal-full-title] Annales d'endocrinologie
  • [ISO-abbreviation] Ann. Endocrinol. (Paris)
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
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44. Tateno T, Izumiyama H, Doi M, Yoshimoto T, Shichiri M, Inoshita N, Oyama K, Yamada S, Hirata Y: Differential gene expression in ACTH -secreting and non-functioning pituitary tumors. Eur J Endocrinol; 2007 Dec;157(6):717-24
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  • [Title] Differential gene expression in ACTH -secreting and non-functioning pituitary tumors.
  • OBJECTIVE: Differential expression of several genes between ACTH-secreting pituitary tumors causing Cushing' disease (CD), silent corticotroph adenoma (SCA), and non-functioning pituitary tumors (NFT) was investigated.
  • DESIGN AND METHODS: We used tissue specimens from 35 pituitary tumors (12 CD, 8 SCA, and 15 NFT).
  • Steady-state mRNA levels of the genes related to proopiomelanocortin (POMC) transcription, synthesis, processing, and secretion, such as neurogenic differentiation 1 (NeuroD1), T-box 19 (Tpit), corticotropin releasing hormone receptor (CRHR), vasopressin receptor 1b (V1bR), prohormone convertase (PC) 1/3 and PC2, 11beta-hydroxysteroid dehydrogenase (11beta-HSD) type 1 and type 2, glucocorticoid receptor alpha (GRalpha), annexin A1, histone deacetylase 2 (HDAC2), and BRM/SWI2-related gene 1, were determined by real-time RT-PCR.
  • In conclusion, our study demonstrated that the genes related to transcription, synthesis, processing, and secretion of POMC are differentially regulated in ACTH-secreting pituitary tumors causing CD and SCA compared with those in NFT.

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  • (PMID = 18057378.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / CRF receptor type 1; 0 / Homeodomain Proteins; 0 / NEUROD1 protein, human; 0 / RNA, Messenger; 0 / Receptors, Corticotropin-Releasing Hormone; 0 / Receptors, Glucocorticoid; 0 / Receptors, Vasopressin; 0 / T-Box Domain Proteins; 0 / TBX19 protein, human; 0 / glucocorticoid receptor alpha; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; EC 1.1.1.146 / 11-beta-Hydroxysteroid Dehydrogenases; EC 3.4.21.94 / Proprotein Convertase 2
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45. Wagenmakers MA, Netea-Maier RT, van Lindert EJ, Timmers HJ, Grotenhuis JA, Hermus AR: Repeated transsphenoidal pituitary surgery (TS) via the endoscopic technique: a good therapeutic option for recurrent or persistent Cushing's disease (CD). Clin Endocrinol (Oxf); 2009 Feb;70(2):274-80
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  • [Title] Repeated transsphenoidal pituitary surgery (TS) via the endoscopic technique: a good therapeutic option for recurrent or persistent Cushing's disease (CD).
  • BACKGROUND: No data on results of repeated transsphenoidal surgery via the endoscopic technique for patients with persistent or recurrent Cushing's disease are available.
  • DESIGN AND PATIENTS: We retrospectively evaluated the remission rates and complications of repeated transsphenoidal surgery via the endoscopic technique in 14 patients with persistent (N = 6) or recurrent (N = 8) Cushing's disease treated in our centre between 1999 and 2007.
  • The success of repeated transsphenoidal surgery could not be predicted by visualization of an adenoma on MRI before first or second surgery, histopathological confirmation of an ACTH secreting adenoma after first or second surgery, treatment with cortisol lowering agents before first or second surgery, the operation technique used during the first surgery, persistent vs. recurrent disease after the first surgery, age, gender and interval between the two surgeries.
  • CONCLUSION: Repeated transsphenoidal surgery via the endoscopic technique is a good treatment option for selected patients with recurrent or persistent Cushing's disease following primary pituitary surgery.
  • [MeSH-major] Endoscopy / methods. Neurosurgical Procedures / methods. Pituitary ACTH Hypersecretion / surgery. Pituitary Gland / surgery

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  • (PMID = 18616702.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] WI4X0X7BPJ / Hydrocortisone
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46. Minniti G, Esposito V, Piccirilli M, Fratticci A, Santoro A, Jaffrain-Rea ML: Diagnosis and management of pituitary tumours in the elderly: a review based on personal experience and evidence of literature. Eur J Endocrinol; 2005 Dec;153(6):723-35
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  • [Title] Diagnosis and management of pituitary tumours in the elderly: a review based on personal experience and evidence of literature.
  • An increasing proportion of pituitary adenomas are recognized in the elderly, raising the question of their optimal diagnosis and management.
  • About 80% of pituitary adenomas in this age group are non-secreting, requiring careful differential diagnosis with non-adenomatous sellar lesions.
  • Recognized secreting tumours are mainly GH-secreting, most of them intrasellar, followed by prolactinomas, which present as clinically non-secreting and are usually invasive.
  • Cushing's disease appears as a very rare eventuality in the elderly.
  • Optimal therapeutic management should aim to control the disease while preserving or improving patient's quality of life.
  • Transsphenoidal surgery has proved to be an efficient and well-tolerated option for non-secreting adenomas with visual defects and intrasellar GH-secreting adenomas, being able to improve metabolic and cardiovascular complications of acromegaly even in this age group.
  • The clinical importance of hypopituitarism should not be underestimated, and thyroid- and adrenal-replacement therapy are mandatory in the presence of documented hormone deficiency, carefully avoiding overtreatment in order to limit possible side effects on the cardiovascular system and bone mineralization.

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  • (PMID = 16322376.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hormones
  • [Number-of-references] 88
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47. Fontana E, Gaillard R: [Epidemiology of pituitary adenoma: results of the first Swiss study]. Rev Med Suisse; 2009 Oct 28;5(223):2172-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Epidemiology of pituitary adenoma: results of the first Swiss study].
  • [Transliterated title] Epidémiologie des adénomes hypophysaires: étude dans une agglomération urbaine de Suisse.
  • Epidemiological data concerning pituitary adenomas are very scarce and in some cases reports are even conflicting.
  • The aim of this study was, therefore, to evaluate in the urban area of Fribourg, the prevalence of relevant clinical pituitary adenoma.
  • General practitioners, endocrinologists and gynaecologists were questioned concerning any patient within this agglomeration presenting with a pituitary micro- or macro-adenoma.
  • Among the 44 adenomas, we observed 13 non secreting macro-adenomas, 16 micro- and 9 macro-prolactinomas, 4 cases of acromegaly and 2 ACTH-dependant Cushing diseases.
  • In the studied area we found a prevalence of 80.5 pituitary adenomas per 100,000, or 1 case per 1241 corroborating a greater prevalence of pituitary adenomas than previously believed.
  • [MeSH-major] Adenoma / epidemiology. Pituitary Neoplasms / epidemiology

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  • (PMID = 19968031.001).
  • [ISSN] 1660-9379
  • [Journal-full-title] Revue médicale suisse
  • [ISO-abbreviation] Rev Med Suisse
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Switzerland
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48. Kawashima ST, Usui T, Sano T, Iogawa H, Hagiwara H, Tamanaha T, Tagami T, Naruse M, Hojo M, Takahashi JA, Shimatsu A: P53 gene mutation in an atypical corticotroph adenoma with Cushing's disease. Clin Endocrinol (Oxf); 2009 Apr;70(4):656-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] P53 gene mutation in an atypical corticotroph adenoma with Cushing's disease.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / complications. ACTH-Secreting Pituitary Adenoma / genetics. Adenoma / genetics. Mutation / genetics. Pituitary ACTH Hypersecretion / etiology. Pituitary Neoplasms / genetics. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 18771563.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
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49. Koutourousiou M, Kontogeorgos G, Wesseling P, Grotenhuis AJ, Seretis A: Collision sellar lesions: experience with eight cases and review of the literature. Pituitary; 2010;13(1):8-17
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  • The concomitant presence of a pituitary adenoma with a second sellar lesion in patients operated upon for pituitary adenoma is an uncommon entity.
  • Although rare, quite a great variety of lesions have been indentified coexisting with pituitary adenomas.
  • In fact, most combinations have been described before, but an overview with information on the frequency of combined pathologies in a large series has not been published.
  • We present a series of eight collision sellar lesions indentified among 548 transsphenoidally resected pituitary adenomas in two Neurosurgical Departments.
  • The histological studies confirmed a case of sarcoidosis within a non-functioning pituitary adenoma, a case of intrasellar schwannoma coexisting with growth hormone (GH) secreting adenoma, two Rathke's cleft cysts combined with pituitary adenomas, three gangliocytomas associated with GH-secreting adenomas, and a case of a double pituitary adenoma.
  • Suggested hypotheses about a common embryonic origin or a potential interaction between pituitary adenomas and the immune system are presented.
  • [MeSH-major] Neoplasms, Second Primary / pathology. Pituitary Neoplasms / pathology. Sella Turcica / pathology
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / pathology. Adult. Aged. Central Nervous System Cysts / pathology. Female. Ganglioneuroma / pathology. Histocytochemistry. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Neurilemmoma / pathology. Retrospective Studies

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  • [Cites] J Clin Neurosci. 2006 Aug;13(7):771-4 [16860986.001]
  • [Cites] Acta Neuropathol. 2006 Jul;112(1):21-8 [16699777.001]
  • [Cites] Acta Neurochir (Wien). 2007 Feb;149(2):201-5; discussion 205-6 [17195046.001]
  • [Cites] Pathol Res Pract. 2007;203(4):221-5 [17395399.001]
  • [Cites] J Endocrinol Invest. 2007 Sep;30(8):677-83 [17923800.001]
  • [Cites] Turk Neurosurg. 2007 Apr;17(2):138-41 [17935032.001]
  • [Cites] Acta Neurochir (Wien). 2007 Dec;149(12):1223-8 [17914599.001]
  • [Cites] Brain Pathol. 2008 Apr;18(2):283-7 [18363939.001]
  • [Cites] Pituitary. 2008;11(3):317-23 [17917812.001]
  • [Cites] Acta Neurochir (Wien). 2009 Dec;151(12):1693-7 [19350200.001]
  • [Cites] Am J Surg Pathol. 2000 Apr;24(4):607-13 [10757410.001]
  • [Cites] Pituitary. 1999 Aug;2(2):123-6 [11081162.001]
  • [Cites] Pituitary. 1999 May;1(3-4):197-205 [11081198.001]
  • [Cites] Pituitary. 1999 May;1(3-4):243-50 [11081204.001]
  • [Cites] Mod Pathol. 2001 Jan;14(1):20-8 [11211306.001]
  • [Cites] J Neurosurg. 2001 Jul;95(1):102-10 [11453377.001]
  • [Cites] Surg Neurol. 2001 May;55(5):284-90 [11516470.001]
  • [Cites] Neuroradiology. 2001 Sep;43(9):755-9 [11594426.001]
  • [Cites] J Korean Med Sci. 2002 Feb;17(1):147-50 [11850608.001]
  • [Cites] Clin Neuropathol. 2002 Mar-Apr;21(2):82-91 [12005257.001]
  • [Cites] Pituitary. 2001 Aug;4(3):195-202 [12138993.001]
  • [Cites] Brain Tumor Pathol. 2002;19(2):63-7 [12622135.001]
  • [Cites] Neurosurgery. 2003 May;52(5):1200-5; discussion 1205-6 [12699566.001]
  • [Cites] J Clin Invest. 2003 Dec;112(11):1603-18 [14660734.001]
  • [Cites] Ann Diagn Pathol. 2004 Jun;8(3):142-50 [15185261.001]
  • [Cites] Minim Invasive Neurosurg. 2004 Aug;47(4):230-4 [15346320.001]
  • [Cites] J Neurosurg. 1966 Jan;24(1):77-81 [5903300.001]
  • [Cites] Cancer. 1978 Jan;41(1):337-43 [626939.001]
  • [Cites] JAMA. 1978 Aug 4;240(5):471-3 [660898.001]
  • [Cites] Horm Res. 1979;10(1):1-13 [218878.001]
  • [Cites] Acta Neurochir (Wien). 1979;48(3-4):191-7 [484274.001]
  • [Cites] J Gerontol. 1980 Jan;35(1):16-22 [6243145.001]
  • [Cites] Arch Pathol Lab Med. 1983 Sep;107(9):488-91 [6309114.001]
  • [Cites] Neurosurgery. 1984 Jan;14(1):71-3 [6694795.001]
  • [Cites] J Clin Endocrinol Metab. 1984 May;58(5):796-803 [6423659.001]
  • [Cites] Neurosurgery. 1987 Sep;21(3):371-7 [3670583.001]
  • [Cites] Surg Neurol. 1988 Oct;30(4):286-92 [3175839.001]
  • [Cites] Endocr Rev. 1988 Aug;9(3):357-73 [3145190.001]
  • [Cites] Exp Clin Endocrinol. 1988 Sep;92(1):69-76 [3229449.001]
  • [Cites] Surg Neurol. 1989 Aug;32(2):156-8 [2749459.001]
  • [Cites] J Neurosurg. 1990 Nov;73(5):731-5 [2213163.001]
  • [Cites] J Clin Endocrinol Metab. 1990 Dec;71(6):1427-33 [1977759.001]
  • [Cites] J Neurosurg. 1991 Feb;74(2):243-7 [1988594.001]
  • [Cites] Acta Neuropathol. 1992;83(2):211-5 [1557952.001]
  • [Cites] Neurosurgery. 1992 Nov;31(5):840-9; discussion 849 [1331847.001]
  • [Cites] Neurosurgery. 1993 Nov;33(5):920-4; discussion 924-5 [8264895.001]
  • [Cites] J Neurosurg. 1994 Jun;80(6):1018-25 [8189257.001]
  • [Cites] Virchows Arch. 1994;425(1):93-9 [7921420.001]
  • [Cites] Ultrastruct Pathol. 1994 Nov-Dec;18(6):565-74 [7855931.001]
  • [Cites] Neurochirurgie. 1994;40(4):263-6 [7753299.001]
  • [Cites] J Clin Endocrinol Metab. 1995 Aug;80(8):2302-11 [7629223.001]
  • [Cites] Arch Pathol Lab Med. 1996 Apr;120(4):369-77 [8619749.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Apr 30;93(9):4240-5 [8633048.001]
  • [Cites] Acta Neurochir (Wien). 1997;139(2):160-1 [9088378.001]
  • [Cites] N Engl J Med. 1997 Apr 24;336(17):1224-34 [9110911.001]
  • [Cites] Neurosurgery. 1998 Jan;42(1):7-16; discussion 16-7 [9442498.001]
  • [Cites] Endocr Rev. 1998 Dec;19(6):798-827 [9861546.001]
  • [Cites] Neurol Neurochir Pol. 1998 Jul-Sep;32(4):987-96 [9864727.001]
  • [Cites] J Comput Assist Tomogr. 1999 Jan-Feb;23(1):34-8 [10050804.001]
  • [Cites] Endocrinology. 2005 Sep;146(9):3985-98 [15932930.001]
  • [Cites] Br J Neurosurg. 2005 Oct;19(5):432-8 [16455568.001]
  • [Cites] J Neurosurg. 2006 Aug;105(2):309-14 [17219839.001]
  • (PMID = 19551516.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 67
  • [Other-IDs] NLM/ PMC2807600
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50. Lodish MB, Sinaii N, Patronas N, Batista DL, Keil M, Samuel J, Moran J, Verma S, Popovic J, Stratakis CA: Blood pressure in pediatric patients with Cushing syndrome. J Clin Endocrinol Metab; 2009 Jun;94(6):2002-8
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  • CONTEXT: Hypertension (HTN) has been reported in up to 60% of children with Cushing syndrome (CS), but its course, side effects, and potential differences among various causes of CS have not been adequately studied.
  • DESIGN: Data from 86 children with corticotropinomas [Cushing disease (CD)] and 27 children with ACTH-independent CS (AICS) were analyzed.

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  • [Cites] Clin Endocrinol (Oxf). 2004 Dec;61(6):768-77 [15579193.001]
  • [Cites] Curr Hypertens Rep. 2004 Dec;6(6):493-9 [15527696.001]
  • [Cites] Pituitary. 2004;7(4):253-6 [16416038.001]
  • [Cites] Best Pract Res Clin Endocrinol Metab. 2006 Sep;20(3):467-82 [16980206.001]
  • [Cites] Pediatrics. 2007 Sep;120(3):e575-86 [17698579.001]
  • [Cites] Nat Clin Pract Endocrinol Metab. 2007 Nov;3(11):748-57 [17955016.001]
  • [Cites] J Clin Endocrinol Metab. 2009 Jan;94(1):1-2 [19126630.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Jan;86(1):117-23 [11231987.001]
  • [Cites] Hypertension. 2000 Nov;36(5):912-6 [11082166.001]
  • [Cites] Semin Nephrol. 2002 Jan;22(1):44-53 [11785068.001]
  • [Cites] J Clin Endocrinol Metab. 2002 May;87(5):2018-23 [11994335.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Jun;88(6):2527-33 [12788849.001]
  • [Cites] Hypertension. 2003 Dec;42(6):1206-52 [14656957.001]
  • [Cites] Metabolism. 1980 Feb;29(2):115-9 [7354720.001]
  • [Cites] J Clin Endocrinol Metab. 1986 Feb;62(2):275-9 [3510223.001]
  • [Cites] Lancet. 1990 Mar 31;335(8692):765-74 [1969518.001]
  • [Cites] Arch Intern Med. 1993 Mar 8;153(5):598-615 [8439223.001]
  • [Cites] Cardiology. 1993;82(2-3):191-222 [8324780.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Jan;78(1):131-7 [7507118.001]
  • [Cites] Clin Endocrinol (Oxf). 1994 Apr;40(4):479-84 [8187313.001]
  • [Cites] N Engl J Med. 1994 Sep 8;331(10):629-36 [8052272.001]
  • [Cites] Am J Hypertens. 1996 Jan;9(1):77-80 [8834710.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Jun;82(6):1734-8 [9177372.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Oct;82(10):3196-202 [9329338.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Aug;84(8):2664-72 [10443657.001]
  • [Cites] Curr Hypertens Rep. 2005 Jun;7(3):212-8 [15913497.001]
  • (PMID = 19293264.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / Z01 HD000642; United States / Intramural NIH HHS / /
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
  • [Other-IDs] NLM/ PMC2690429
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51. Saeger W: [Effects of irradiation therapy and inhibiting drugs on the pituitary and its adenomas]. Pathologe; 2006 Feb;27(1):57-60
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  • [Title] [Effects of irradiation therapy and inhibiting drugs on the pituitary and its adenomas].
  • Radiation therapies of pituitary adenomas induce an increase in fibroses and nuclear pleomorphism.
  • Most growth hormone (GH) secreting pituitary adenomas react to somatostatin analogues by a distinct decrease of GH secretion.
  • Some cases show a shrinkage of adenomas that correlates with fibrosis of the tumor.
  • With these drugs, thyroid stimulating hormone secreting adenomas can also be treated.
  • Prolactin secreting adenomas are mostly treated primarily with dopamine agonists.
  • Up to 90% of cases show a strong decrease in hormone secretion and a distinct shrinkage of the adenomas based on strong decrease in adenoma cell volume.
  • Long-term medication with high doses of glucocorticoids induces Crooke's cells in the anterior pituitary.
  • These are suppressed ACTH cells and characterized by increased numbers of large lysosomes and dense bundles of cytofilaments.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Pituitary Gland / pathology. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / radiotherapy. Radiotherapy / adverse effects

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  • [Cites] Endocrine. 2004 Nov;25(2):141-5 [15711028.001]
  • [Cites] Endocr Pathol. 2000 Winter;11(4):341-352 [12114758.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Jul;87(7):3013-8 [12107192.001]
  • [Cites] Pathol Res Pract. 1986 Jun;181(3):280-90 [3748874.001]
  • [Cites] Histol Histopathol. 1987 Apr;2(2):135-42 [2980713.001]
  • [Cites] Ultrastruct Pathol. 2005 May-Aug;29(3-4):163-7 [16036872.001]
  • [Cites] Endocrine. 2001 Apr;14(3):329-36 [11444429.001]
  • [Cites] Pathol Res Pract. 1993 Nov;189(9):1044-51 [8302723.001]
  • [Cites] Exp Clin Endocrinol. 1992;100(3):106-11 [1305059.001]
  • [Cites] Acta Endocrinol (Copenh). 1991 Apr;124(4):487-91 [2031445.001]
  • [Cites] Mayo Clin Proc. 1997 Oct;72(10):893-900 [9379690.001]
  • [Cites] J Neurooncol. 2001 Sep;54(2):151-66 [11761432.001]
  • [Cites] Microsc Res Tech. 1992 Jan 15;20(2):162-76 [1547357.001]
  • [Cites] Exp Clin Endocrinol. 1988 Sep;92(1):59-68 [2906615.001]
  • (PMID = 16362259.001).
  • [ISSN] 0172-8113
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Dopamine Agonists; 0 / Glucocorticoids
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52. Tateno T, Izumiyama H, Doi M, Akashi T, Ohno K, Hirata Y: Defective expression of prohormone convertase 1/3 in silent corticotroph adenoma. Endocr J; 2007 Dec;54(5):777-82
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  • [Title] Defective expression of prohormone convertase 1/3 in silent corticotroph adenoma.
  • Silent corticotroph adenoma (SCA) is defined as an ACTH-producing pituitary tumor not associated with clinical and endocrine feartures of Cushing's syndrome, but its underlying molecular mechanism(s) remains unknown thus far.
  • We tested the hypothesis that reduced expression of prohormone convertase (PC) 1/3 responsible for proteolytic processing of proopiomelanocortin (POMC) in SCA may lead to production of unprocessed, biologically inactive POMC and/or precursor of ACTH.
  • Among 30 non-functioning pituitary macroadenomas (NFA) examined, we found 6 SCAs by immunohistochemical study using anti-ACTH antibody.
  • Preoperative endocrine and diagnostic image tests did not reveal any differences between SCA and the remaining NFA except for the higher recurrence rate of SCA.
  • Our data suggest that defective PC1/3 expression may lead to preferential production of unprocessed, biologically inactive ACTH variants in SCA.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / genetics. Adenoma / genetics. Proprotein Convertase 1 / genetics

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  • (PMID = 17917309.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Protein Isoforms; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; EC 3.4.21.93 / Proprotein Convertase 1
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53. Giacomini D, Páez-Pereda M, Theodoropoulou M, Gerez J, Nagashima AC, Chervin A, Berner S, Labeur M, Refojo D, Renner U, Stalla GK, Arzt E: Bone morphogenetic protein-4 control of pituitary pathophysiology. Front Horm Res; 2006;35:22-31
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  • [Title] Bone morphogenetic protein-4 control of pituitary pathophysiology.
  • Bone morphogenetic protein-4 (BMP-4), a member of the transforming growth factor-Beta(TGF-Beta) family, is overexpressed in different prolactinoma models and induces the development of these lineage adenomas.
  • SMAD proteins activated by growth factors of the TGF-Beta and BMP family interact with estrogen receptors to stimulate the proliferation of prolactin and growth hormone-secreting cells.
  • Furthermore, BMP-4 presents differential expression in normal and adenomatous corticotropes and inhibitory action on corticotropinoma cell proliferation.
  • The present review highlights not only the crucial and opposite role of BMP-4 in the progression of pituitary adenomas but also that BMP-4 and retinoic acid interaction might serve as a potential new mechanism target for therapeutic approaches for Cushing disease.
  • [MeSH-major] Bone Morphogenetic Proteins / physiology. Pituitary Diseases / etiology
  • [MeSH-minor] Adrenocorticotropic Hormone / secretion. Animals. Bone Morphogenetic Protein 4. Gene Expression. Humans. Models, Biological. Neurons / secretion. Pituitary Gland / cytology. Pituitary Gland / growth & development. Pituitary Gland / metabolism. Pituitary Gland / secretion. Receptors, Transforming Growth Factor beta / metabolism. Transforming Growth Factor beta / physiology. Tretinoin / pharmacology

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  • (PMID = 16809920.001).
  • [ISSN] 0301-3073
  • [Journal-full-title] Frontiers of hormone research
  • [ISO-abbreviation] Front Horm Res
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / BMP4 protein, human; 0 / Bone Morphogenetic Protein 4; 0 / Bone Morphogenetic Proteins; 0 / Receptors, Transforming Growth Factor beta; 0 / Transforming Growth Factor beta; 5688UTC01R / Tretinoin; 9002-60-2 / Adrenocorticotropic Hormone
  • [Number-of-references] 42
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54. Ewing I, Pedder-Smith S, Franchi G, Ruscica M, Emery M, Vax V, Garcia E, Czirják S, Hanzély Z, Kola B, Korbonits M, Grossman AB: A mutation and expression analysis of the oncogene BRAF in pituitary adenomas. Clin Endocrinol (Oxf); 2007 Mar;66(3):348-52
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  • [Title] A mutation and expression analysis of the oncogene BRAF in pituitary adenomas.
  • We speculated that this same gene may be either mutated at this site, or overexpressed, in pituitary adenomas.
  • DESIGN AND MEASUREMENTS: We sequenced 37 pituitary adenomas for a mutation at the V600E position.
  • In addition, we investigated B-Raf mRNA expression in normal pituitary (n = 5) and nonfunctioning pituitary adenomas (NFPA) (n = 6) by semiquantitative PCR, and in a further 27 pituitary adenomas of various types and 10 normal pituitaries using real-time quantitative PCR.
  • B-Raf mRNA was overexpressed in pituitary adenomas compared to normal pituitary, and this was entirely due to overexpression in NFPAs.
  • CONCLUSIONS: Mutations previously seen in the majority of melanomas and a substantial minority of papillary thyroid carcinomas are not a frequent finding in pituitary adenomas.
  • [MeSH-major] Adenoma / chemistry. DNA Mutational Analysis. Gene Expression Regulation, Neoplastic. Pituitary Neoplasms / chemistry. Proto-Oncogene Proteins B-raf / genetics. RNA, Messenger / analysis
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / chemistry. Case-Control Studies. Growth Hormone-Secreting Pituitary Adenoma / chemistry. Humans. Polymerase Chain Reaction / methods. Prolactinoma / chemistry. Statistics, Nonparametric

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  • (PMID = 17302867.001).
  • [ISSN] 0300-0664
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf
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55. Er U, Gürses L, Saka C, Belen D, Yiğitkanli K, Simşek S, Akin I, Bavbek M: Sublabial transseptal approach to pituitary adenomas with special emphasis on rhinological complications. Turk Neurosurg; 2008 Oct;18(4):425-30
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  • [Title] Sublabial transseptal approach to pituitary adenomas with special emphasis on rhinological complications.
  • OBJECTIVE: The aim of this presentation is to show that the sublabial transseptal transsphenoidal approach to pituitary adenomas is the least invasive anatomic route with the lowest postoperative complication rates.
  • PATIENTS AND METHOD: This study was based on a retrospective analysis of 276 patients with a diagnosis of pituitary adenoma who were surgically treated via the sublabial transsphenoidal route.
  • [MeSH-major] Adenoma / surgery. Neurosurgical Procedures / methods. Nose Diseases / epidemiology. Nose Diseases / etiology. Pituitary Neoplasms / surgery. Postoperative Complications / epidemiology
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / surgery. Adult. Aged. Diabetes Insipidus / epidemiology. Diabetes Insipidus / etiology. Female. Growth Hormone-Secreting Pituitary Adenoma / surgery. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Nasal Mucosa / injuries. Nasal Mucosa / pathology. Nasal Septum / injuries. Nasal Septum / pathology. Neoplasm Recurrence, Local / epidemiology. Prolactinoma / surgery. Retrospective Studies. Thyrotropin / metabolism. Tomography, X-Ray Computed. Treatment Outcome. Water-Electrolyte Imbalance / epidemiology. Water-Electrolyte Imbalance / etiology. Young Adult


56. Gallelli MF, Cabrera Blatter MF, Castillo V: A comparative study by age and gender of the pituitary adenoma and ACTH and alpha-MSH secretion in dogs with pituitary-dependent hyperadrenocorticism. Res Vet Sci; 2010 Feb;88(1):33-40
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  • [Title] A comparative study by age and gender of the pituitary adenoma and ACTH and alpha-MSH secretion in dogs with pituitary-dependent hyperadrenocorticism.
  • Pituitary-dependent hyperadrenocorticism (PDH) is frequent in dogs.
  • Using magnetic resonance, pituitary tumours were intra-sellar (IS) in 30.8% and extra-sellar (ES) in 62.6% and the pars intermedia (PI) was affected in 6.5%.
  • ACTH concentration was greater in the ES vs. IS (p<0.05).
  • alpha-MSH did not present significant differences according to tumour size, showing a negative correlation (r=-0.47; p<0.01) vs. ACTH.
  • Differences in adenoma size according to gender and their age-related frequency of apparition could be because of different origins of the corticotrophinoma.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / veterinary. Adrenocortical Hyperfunction / veterinary. Adrenocorticotropic Hormone / secretion. Dog Diseases / pathology. Pituitary Neoplasms / veterinary. alpha-MSH / secretion
  • [MeSH-minor] Age Factors. Animals. Dogs. Female. Magnetic Resonance Imaging. Male. Pituitary Gland / pathology. Pituitary Gland / physiopathology. Pituitary Gland / secretion. Retrospective Studies. Sex Factors

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  • [Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19683322.001).
  • [ISSN] 1532-2661
  • [Journal-full-title] Research in veterinary science
  • [ISO-abbreviation] Res. Vet. Sci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 581-05-5 / alpha-MSH; 9002-60-2 / Adrenocorticotropic Hormone
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57. Barber TM, Adams E, Ansorge O, Byrne JV, Karavitaki N, Wass JA: Nelson's syndrome. Eur J Endocrinol; 2010 Oct;163(4):495-507
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  • Nelson's syndrome is a potentially life-threatening condition that does not infrequently develop following total bilateral adrenalectomy (TBA) for the treatment of Cushing's disease.
  • In this review article, we discuss some controversial aspects of Nelson's syndrome including diagnosis, predictive factors, aetiology, pathology and management based on data from the existing literature and the experience of our own tertiary centre.
  • We propose that Nelson's syndrome should be diagnosed in any patient with prior TBA for the treatment of Cushing's disease and with at least one of the following criteria: i) an expanding pituitary mass lesion compared with pre-TBA images;.
  • ii) an elevated 0800 h plasma level of ACTH (>500 ng/l) in addition to progressive elevations of ACTH (a rise of >30%) on at least three consecutive occasions.
  • Regarding predictive factors for the development of Nelson's syndrome post TBA, current evidence favours the presence of residual pituitary tumour on magnetic resonance imaging (MRI) post transsphenoidal surgery (TSS); an aggressive subtype of corticotrophinoma (based on MRI growth rapidity and histology of TSS samples); lack of prophylactic neoadjuvant pituitary radiotherapy at the time of TBA and a rapid rise of ACTH levels in year 1 post TBA.
  • Finally, more studies are needed to assess the efficacy of therapeutic strategies in Nelson's syndrome, including the alkylating agent, temozolomide, which holds promise as a novel and effective therapeutic agent in the treatment of associated aggressive corticotroph tumours.

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  • (PMID = 20668020.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Alkylating Agents; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; 9002-60-2 / Adrenocorticotropic Hormone
  • [Number-of-references] 101
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58. Mayberg M, Vermeulen S: Advances in stereotactic radiosurgery in the treatment of pituitary adenomas. Curr Opin Endocrinol Diabetes Obes; 2007 Aug;14(4):296-300
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  • [Title] Advances in stereotactic radiosurgery in the treatment of pituitary adenomas.
  • PURPOSE OF REVIEW: Stereotactic radiosurgery has become the preferred radiation treatment modality for secreting and nonsecreting pituitary adenomas, although randomized studies comparing delivery systems, fractionation and dose have not been performed.
  • With a reduction in acute and chronic side effects, the total dose to abnormal tissue can be increased allowing for greater tumor control.
  • SUMMARY: The radiobiology, control rates and normal tissue tolerances of stereotactic radiosurgery in the treatment of pituitary adenomas is reviewed.
  • [MeSH-major] Adenoma / surgery. Pituitary Neoplasms / surgery. Radiosurgery
  • [MeSH-minor] Acromegaly / radiotherapy. Acromegaly / surgery. Humans. Pituitary ACTH Hypersecretion / radiotherapy. Pituitary ACTH Hypersecretion / surgery. Prolactinoma / surgery. Prolactinoma / therapy

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  • (PMID = 17940455.001).
  • [ISSN] 1752-2978
  • [Journal-full-title] Current opinion in endocrinology, diabetes, and obesity
  • [ISO-abbreviation] Curr Opin Endocrinol Diabetes Obes
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 18
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59. Rudnik A, Zawadzki T, Gałuszka-Ignasiak B, Bazowski P, Duda I, Wojtacha M, Rudnik AI, Krawczyk I: Endoscopic transsphenoidal treatment in recurrent and residual pituitary adenomas--first experience. Minim Invasive Neurosurg; 2006 Feb;49(1):10-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Endoscopic transsphenoidal treatment in recurrent and residual pituitary adenomas--first experience.
  • AIM OF THE STUDY: The aim of the study has been the assessment of the endoscopic method in the surgical management of recurrent and residual pituitary adenomas, as concerns treatment efficiency, substantial complications, and its possible advantages for the operating surgeon and patient.
  • MATERIAL AND METHODS: In Department of Neurosurgery, Silesian University School of Medicine in Katowice, between October 2001 and June 2004, 125 patients underwent endoscopic surgery due to pituitary adenoma.
  • The analysis comprised 20 patients, who were operated on due to recurrent adenomas or residual tumour not completely removed during the first surgical procedure.
  • The analysed group had 14 non-functioning adenomas, 4 GH-secreting adenomas, 1 PRL-secreting adenoma and 1 ACTH-secreting adenoma.
  • 11 of the 20 adenomas infiltrated the cavernous sinuses.
  • In the group of 11 patients with adenomas not infiltrating the cavernous sinuses, recovery was reported for 8 of them, that is 73%.
  • CONCLUSIONS: The endoscopic method is a safe, hardly invasive and efficient surgical technique in the treatment of recurrent and residual pituitary adenomas.
  • [MeSH-major] Adenoma / surgery. Neoplasm Recurrence, Local / surgery. Neuroendoscopy. Pituitary Neoplasms / surgery. Sphenoid Sinus / surgery
  • [MeSH-minor] Adult. Aged. Female. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm, Residual. Reoperation. Treatment Outcome

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  • (PMID = 16547875.001).
  • [ISSN] 0946-7211
  • [Journal-full-title] Minimally invasive neurosurgery : MIN
  • [ISO-abbreviation] Minim Invasive Neurosurg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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60. Banasiak MJ, Malek AR: Nelson syndrome: comprehensive review of pathophysiology, diagnosis, and management. Neurosurg Focus; 2007;23(3):E13
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nelson syndrome: comprehensive review of pathophysiology, diagnosis, and management.
  • Nelson syndrome (NS) is a rare clinical manifestation of an enlarging pituitary adenoma that can occur following bilateral adrenal gland removal performed for the treatment of Cushing disease.
  • It is characterized by excess adreno-corticotropin secretion and hyperpigmentation of the skin and mucus membranes.
  • The authors present a comprehensive review of the pathophysiology, diagnosis, and management of NS.
  • Corticotroph adenomas in NS remain challenging tumors that can lead to significant rates of morbidity and mortality.
  • Although the primary treatment for each tumor type may vary, it is important to consider all of the available options and select the one that is most appropriate for the individual case, particularly in cases of lesions resistant to intervention.


61. Castinetti F, Nagai M, Morange I, Dufour H, Caron P, Chanson P, Cortet-Rudelli C, Kuhn JM, Conte-Devolx B, Regis J, Brue T: Long-term results of stereotactic radiosurgery in secretory pituitary adenomas. J Clin Endocrinol Metab; 2009 Sep;94(9):3400-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term results of stereotactic radiosurgery in secretory pituitary adenomas.
  • OBJECTIVE: The aim of the study was to determine long-term efficacy and adverse effects of SR in secreting pituitary adenomas.
  • PATIENTS: A total of 76 patients were treated by SR for acromegaly (n = 43), Cushing's disease (CD; n = 18), or prolactinoma (n = 15) as a primary (n = 27) or adjunctive postsurgical treatment (n = 49).
  • CONCLUSIONS: SR is an effective and safe primary or adjunctive treatment in selected patients with secreting pituitary adenomas.
  • [MeSH-major] Adenoma / surgery. Pituitary Neoplasms / surgery. Radiosurgery
  • [MeSH-minor] Acromegaly / surgery. Adolescent. Adrenocorticotropic Hormone / secretion. Adult. Aged. Child. Female. Human Growth Hormone / secretion. Humans. Male. Middle Aged. Pituitary ACTH Hypersecretion / surgery. Prolactin / secretion. Prolactinoma / surgery. Retrospective Studies


62. Colao A, Pivonello R, Di Somma C, Savastano S, Grasso LF, Lombardi G: Medical therapy of pituitary adenomas: effects on tumor shrinkage. Rev Endocr Metab Disord; 2009 Jun;10(2):111-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Medical therapy of pituitary adenomas: effects on tumor shrinkage.
  • The efficacy of dopamine-agonists (DA) in patients with prolactinomas and that of somatostatin analogues (SSA) in those with GH- and TSH-secreting adenomas is well established.
  • More recently, data are accumulating suggesting a potential therapeutic role of DA also in patients with ACTH-secreting and clinically non-functioning (NFA) pituitary adenomas.
  • This review aims at summarizing published results of DA and SSA on tumor shrinkage in patients with different histotypes of pituitary adenomas.
  • Results of tumor shrinkage are of clinical relevance as tumor size is the one of the most important determinant of surgical outcome.
  • While reduction of tumor size more than 50% of baseline size in macroprolactinomas treated with DA is a frequent finding in patients with GH-secreting adenomas treated with SSA tumor shrinkage only recently is becoming frequent thanks to the availability of depot formulations.
  • Data on tumor shrinkage in patients with TSH-secreting adenomas treated with SSA are limited because of the rarity of these tumors.
  • Very recently, DA have been reported of some efficacy also in patients with ACTH-secreting adenomas but data are still very limited.
  • [MeSH-major] Hormones / therapeutic use. Pituitary Neoplasms / drug therapy. Somatostatin / analogs & derivatives. Somatostatin / therapeutic use

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  • (PMID = 18791829.001).
  • [ISSN] 1573-2606
  • [Journal-full-title] Reviews in endocrine & metabolic disorders
  • [ISO-abbreviation] Rev Endocr Metab Disord
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Hormones; 51110-01-1 / Somatostatin; 9002-60-2 / Adrenocorticotropic Hormone; 9002-71-5 / Thyrotropin; 9002-72-6 / Growth Hormone
  • [Number-of-references] 103
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63. Hanson JM, Mol JA, Leegwater PA, Bilodeau S, Drouin J, Meij BP: Expression and mutation analysis of Tpit in the canine pituitary gland and corticotroph adenomas. Domest Anim Endocrinol; 2008 Apr;34(3):217-22
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  • [Title] Expression and mutation analysis of Tpit in the canine pituitary gland and corticotroph adenomas.
  • Pituitary-dependent hyperadrenocorticism (PDH) in dogs is caused by a pituitary corticotroph adenoma.
  • Although PDH is a common disorder in dogs, little is known about the underlying pathogenesis.
  • In the pituitary glands of humans and mice, the pro-opiomelanocortin (POMC)-expressing cell lineages, the corticotrophs and melanotrophs, have a specific marker in common, the T-box transcription factor Tpit (Tbx19), which is obligate for POMC expression.
  • Tpit also regulates the late differentiation of the corticotrophs and melanotrophs, and therefore may contribute to the pathogenesis of the corticotroph adenomas.
  • The aim of this study was to perform an expression and mutation analysis of Tpit in the normal canine pituitary and in corticotroph adenomas.
  • The distribution of the Tpit protein in the pituitary gland was studied with immunohistochemistry and the expression of the gene with RT-PCR.
  • Tpit was expressed in corticotroph and melanotroph cells of the normal and adenomatous canine pituitary, and remained present in non-adenomatous corticotrophs of pituitaries from PDH dogs.
  • No tumor-specific mutation in the Tpit cDNA from the corticotroph adenomas was found.
  • It is concluded that Tpit can be used as a reliable marker for the corticotroph and melanotroph cells in the canine pituitary tissue and that mutations in the Tpit gene are unlikely to play a major role in the pathogenesis of canine corticotroph adenomas.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / veterinary. Adenoma / veterinary. Dog Diseases / genetics. Pituitary Gland / chemistry. Pituitary Neoplasms / veterinary. T-Box Domain Proteins / genetics

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  • (PMID = 17544240.001).
  • [ISSN] 0739-7240
  • [Journal-full-title] Domestic animal endocrinology
  • [ISO-abbreviation] Domest. Anim. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / T-Box Domain Proteins; 9007-49-2 / DNA
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64. Nandagopal R, Vortmeyer A, Oldfield EH, Keil MF, Stratakis CA: Cushing's syndrome due to a pituitary corticotropinoma in a child with tuberous sclerosis: an association or a coincidence? Clin Endocrinol (Oxf); 2007 Oct;67(4):639-41
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  • [Title] Cushing's syndrome due to a pituitary corticotropinoma in a child with tuberous sclerosis: an association or a coincidence?
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / complications. Cushing Syndrome / etiology. Pituitary Neoplasms / complications. Tuberous Sclerosis / complications


65. Saveanu A, Gunz G, Guillen S, Dufour H, Culler MD, Jaquet P: Somatostatin and dopamine-somatostatin multiple ligands directed towards somatostatin and dopamine receptors in pituitary adenomas. Neuroendocrinology; 2006;83(3-4):258-63
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  • [Title] Somatostatin and dopamine-somatostatin multiple ligands directed towards somatostatin and dopamine receptors in pituitary adenomas.
  • AIM: We report the comparative efficacy of octreotide, cabergoline and multiple ligands directed towards the different somatostatin subtypes (ssts), such as BIM-23A779 and SOM-230, and of chimeric analogs which bind both somatostatin and the dopamine D2 receptors (D2R), such as BIM-23A760 and BIM-23A781, in cell cultures from human growth hormone (GH)-secreting pituitary adenomas.
  • PROCEDURES: RT-PCR analysis of the quantitative expression of the different ssts and D2R mRNAs was performed on tumor fragments of 22 GH-secreting adenomas collected after surgery.
  • Pharmacological studies, using the different ligands, were performed on cell cultures of such tumors.
  • In each tumor tested, 3 patterns of response, in terms of GH suppression, were observed.
  • Among the compounds tested, the most potent inhibitors of GH secretion were the sst2, sst5, D2R chimeric compound BIM-23A760, followed by the sst universal ligand SOM-230.
  • The effect of multiple receptor activation on the functions of other pituitary tumor types, such as prolactinomas and corticotropinomas, is not presently analyzed, and the efficacy of multireceptor ligands remains to be elucidated.
  • [MeSH-major] Adenoma / drug therapy. Antineoplastic Agents, Hormonal / therapeutic use. Dopamine / analogs & derivatives. Pituitary Neoplasms / drug therapy. Somatostatin / analogs & derivatives
  • [MeSH-minor] Adult. Drug Screening Assays, Antitumor. Ergolines / therapeutic use. Female. Human Growth Hormone / drug effects. Human Growth Hormone / metabolism. Humans. Ligands. Male. Octreotide / therapeutic use. RNA, Messenger / analysis. Receptors, Dopamine D2 / drug effects. Receptors, Dopamine D2 / genetics. Receptors, Dopamine D2 / metabolism. Receptors, Somatostatin / classification. Receptors, Somatostatin / drug effects. Receptors, Somatostatin / genetics. Receptors, Somatostatin / metabolism. Recombinant Fusion Proteins / therapeutic use. Tumor Cells, Cultured

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  • (PMID = 17047391.001).
  • [ISSN] 0028-3835
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / BIM 23268; 0 / Ergolines; 0 / Ligands; 0 / RNA, Messenger; 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin; 0 / Recombinant Fusion Proteins; 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin; LL60K9J05T / cabergoline; RWM8CCW8GP / Octreotide; VTD58H1Z2X / Dopamine
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66. Roelfsema F, Kok S, Kok P, Pereira AM, Biermasz NR, Smit JW, Frolich M, Keenan DM, Veldhuis JD, Romijn JA: Pituitary-hormone secretion by thyrotropinomas. Pituitary; 2009;12(3):200-10
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  • [Title] Pituitary-hormone secretion by thyrotropinomas.
  • Hormone secretion by somatotropinomas, corticotropinomas and prolactinomas exhibits increased pulse frequency, basal and pulsatile secretion, accompanied by greater disorderliness.
  • Regulation of non-TSH pituitary hormones in this context is not well understood.
  • Cross-ApEn synchrony between TSH and GH did not differ between patients and controls, but TSH and PRL synchrony was reduced in patients.
  • We conclude that TSH secretion by thyrotropinomas shares many characteristics of other pituitary hormone-secreting adenomas.
  • In addition, abnormalities in GH and PRL secretion exist ranging from decreased (joint) regularity to overt hypersecretion, although not always clinically obvious, suggesting tumoral transformation of thyrotrope lineage cells.
  • [MeSH-major] Adenoma / physiopathology. Pituitary Hormones / blood. Pituitary Hormones / secretion. Pituitary Neoplasms / blood

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  • [Cites] Eur J Endocrinol. 1994 Oct;131(4):331-40 [7921220.001]
  • [Cites] J Clin Invest. 1994 Sep;94(3):1277-88 [8083369.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Dec;79(6):1706-15 [7989479.001]
  • [Cites] J Clin Endocrinol Metab. 1995 Aug;80(8):2518-22 [7543115.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Nov 26;93(24):14100-5 [8943067.001]
  • [Cites] Endocr Rev. 1996 Dec;17(6):610-38 [8969971.001]
  • [Cites] Clin Endocrinol (Oxf). 1997 Nov;47(5):599-612 [9425400.001]
  • [Cites] Thyroid. 1998 Jan;8(1):9-14 [9492147.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Feb;84(2):476-86 [10022404.001]
  • [Cites] Eur J Endocrinol. 1999 Mar;140(3):192-200 [10216513.001]
  • [Cites] Am J Physiol Regul Integr Comp Physiol. 2005 Feb;288(2):R440-6 [15486096.001]
  • [Cites] Clin Endocrinol (Oxf). 2005 Feb;62(2):176-81 [15670193.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Mar;90(3):1570-7 [15598691.001]
  • [Cites] Am J Physiol Endocrinol Metab. 2005 Jul;289(1):E160-5 [15727954.001]
  • [Cites] Tissue Cell. 2005 Aug;37(4):269-80 [15921714.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Nov;90(11):6185-91 [16091498.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Nov 15;102(46):16880-5 [16272219.001]
  • [Cites] Eur J Endocrinol. 2007 Jul;157(1):39-46 [17609400.001]
  • [Cites] J Neuroendocrinol. 2008 Jan;20(1):1-70 [18081553.001]
  • [Cites] J Neurosurg. 2008 Jul;109(1):17-22 [18590428.001]
  • [Cites] J Neuroendocrinol. 2008 Jun;20(6):687-91 [18601690.001]
  • [Cites] Am J Physiol Regul Integr Comp Physiol. 2003 Sep;285(3):R664-73 [12738612.001]
  • [Cites] J Clin Endocrinol Metab. 2004 May;89(5):2290-300 [15126555.001]
  • [Cites] Am J Physiol. 1999 Nov;277(5 Pt 1):E948-57 [10567024.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Apr;85(4):1487-91 [10770186.001]
  • [Cites] Methods Enzymol. 2000;321:149-82 [10909056.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Feb;86(2):700-12 [11158034.001]
  • [Cites] Am J Physiol Regul Integr Comp Physiol. 2001 Mar;280(3):R721-9 [11171650.001]
  • [Cites] Am J Physiol Regul Integr Comp Physiol. 2001 Jun;280(6):R1755-71 [11353681.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Jun;86(6):2849-53 [11397898.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Jul;86(7):3304-10 [11443205.001]
  • [Cites] Mol Endocrinol. 2001 Sep;15(9):1529-38 [11518802.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Nov;86(11):5572-6 [11701737.001]
  • [Cites] Rev Endocr Metab Disord. 2000 Jan;1(1-2):97-108 [11704998.001]
  • [Cites] J Neurooncol. 2001 Sep;54(2):179-86 [11761434.001]
  • [Cites] Ultrastruct Pathol. 2002 Jul-Aug;26(4):219-28 [12227947.001]
  • [Cites] Eur J Endocrinol. 2003 Apr;148(4):433-42 [12656664.001]
  • [Cites] Clin Endocrinol (Oxf). 2004 Jun;60(6):765-72 [15163342.001]
  • [Cites] Acta Neuropathol. 2004 Aug;108(2):147-53 [15185102.001]
  • [Cites] J Clin Endocrinol Metab. 1987 Aug;65(2):315-20 [3597710.001]
  • [Cites] Acta Neuropathol. 1988;76(5):458-64 [2847475.001]
  • [Cites] J Clin Endocrinol Metab. 1989 Jun;68(6):1211-5 [2723029.001]
  • [Cites] J Clin Endocrinol Metab. 1990 Jun;70(6):1631-6 [2347898.001]
  • [Cites] J Clin Endocrinol Metab. 1990 Dec;71(6):1616-23 [2172282.001]
  • [Cites] J Clin Endocrinol Metab. 1991 Feb;72(2):415-21 [1704010.001]
  • [Cites] J Clin Endocrinol Metab. 1991 Feb;72(2):477-83 [1704011.001]
  • [Cites] J Clin Endocrinol Metab. 1991 Dec;73(6):1281-8 [1955510.001]
  • [Cites] Clin Endocrinol (Oxf). 1992 Dec;37(6):504-10 [1286520.001]
  • [Cites] Ann Intern Med. 1993 Aug 1;119(3):236-40 [8323093.001]
  • [Cites] Eur J Endocrinol. 1994 Feb;130(2):113-20 [8130883.001]
  • [Cites] Eur J Endocrinol. 1994 Oct;131(4):355-8 [7921223.001]
  • (PMID = 19051037.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / M01 RR000585
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Pituitary Hormones; 67763-96-6 / Insulin-Like Growth Factor I; 9002-62-4 / Prolactin; 9002-71-5 / Thyrotropin; 9002-72-6 / Growth Hormone
  • [Other-IDs] NLM/ PMC2712623
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67. Castillo VA, Gómez NV, Lalia JC, Cabrera Blatter MF, García JD: Cushing's disease in dogs: cabergoline treatment. Res Vet Sci; 2008 Aug;85(1):26-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cushing's disease in dogs: cabergoline treatment.
  • The treatment of pituitary-dependent hyperadrenocorticism (PDH) in dogs has for a long time been focused on inhibiting the adrenal gland using drugs such as o-p'-DDD, Ketoconazole and Trilostane, without attacking the primary cause: the corticotrophinoma.
  • Corticotroph cells can express the D2 dopaminergic receptor; therefore cabergoline (Cbg) could be effective as a treatment.
  • A year after the treatment, there was a significant decrease in ACTH (p<0.0001), alpha-MSH (p<0.01), urinary cortisol/creatinine ratio (p<0.001), and of the tumor size (p<0.0001) evaluated by nuclear magnetic resonance.
  • [MeSH-major] Dog Diseases / drug therapy. Dopamine Agonists / therapeutic use. Ergolines / therapeutic use. Pituitary ACTH Hypersecretion / veterinary

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  • (PMID = 17910968.001).
  • [ISSN] 0034-5288
  • [Journal-full-title] Research in veterinary science
  • [ISO-abbreviation] Res. Vet. Sci.
  • [Language] eng
  • [Publication-type] Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Ergolines; 581-05-5 / alpha-MSH; 9002-60-2 / Adrenocorticotropic Hormone; LL60K9J05T / cabergoline; R9400W927I / Ketoconazole
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68. Gao C, Fu X, Pan Y, Li Q: Surgical treatment of pancreatic neuroendocrine tumors: report of 112 cases. Dig Surg; 2010 Aug;27(3):197-204
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVES: To review the clinical data of a group of patients with pancreatic neuroendocrine tumors (pNETs) and to investigate the role of surgery in the treatment for pNETs by analyzing clinical manifestations and postoperative course of this rare disease.
  • Patients' data related to demographics and characteristics, diagnostic studies, surgical and tumor characteristics and survival were retrospectively reviewed.
  • RESULTS: Forty-six patients (41.1%) had a well-differentiated neuroendocrine tumor (WDT), 44 (48.2%) a well-differentiated neuroendocrine carcinoma (WD-Ca) and 12 (10.7%) a poorly differentiated neuroendocrine carcinoma (PD-Ca).
  • Nonfunctional tumors were seen in 65 (58.0%) patients, whereas functional tumors were found in 47 (42.0%) patients, including 26 insulinomas, 17 gastrinomas, 2 VIPomas, 1 glucagonoma, and 1 ACTHoma.
  • Survival was significantly related to the type of neuroendocrine tumor (p = 0.001).
  • The 5-year survival rate differed significantly between patients with tumor node metastasis (TNM) stage I and II disease and those with stage III and IV tumors (p = 0.011).
  • Malignant cases should be treated with aggressive radical surgery to achieve complete tumor resection and potential for long-term survival.

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  • (PMID = 20571266.001).
  • [ISSN] 1421-9883
  • [Journal-full-title] Digestive surgery
  • [ISO-abbreviation] Dig Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
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69. Chowdhury IN, Sinaii N, Oldfield EH, Patronas N, Nieman LK: A change in pituitary magnetic resonance imaging protocol detects ACTH-secreting tumours in patients with previously negative results. Clin Endocrinol (Oxf); 2010 Apr;72(4):502-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A change in pituitary magnetic resonance imaging protocol detects ACTH-secreting tumours in patients with previously negative results.
  • OBJECTIVE: While detection of pituitary tumours with magnetic resonance imaging (MRI) may reduce diagnostic costs and improve surgical outcomes for patients with Cushing's disease, the optimal T1-weighted spin-echo (SE) MRI protocol remains unknown.
  • We hypothesized that specific MR scanning parameters influence detection of corticotropinomas.
  • DESIGN AND PATIENTS: Between December 1997 and November 2004, 21 of 84 consecutive patients with Cushing's disease had a falsely negative initial pituitary MRI study and a lesion identified subsequently at the National Institutes of Health Clinical Center.
  • This study retrospectively reviewed and compared technical parameters used for the two pituitary T1-weighted SE MRIs in 18 patients with available scans.
  • Immunohistochemistry of tumours resected at transsphenoidal surgery confirmed all to be corticotropinomas.
  • CONCLUSIONS: Not all 'T1-weighted SE' scans are equally accurate.
  • We recommend that endocrinologists consider pituitary MRI parameters when interpreting the results.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / diagnosis. Magnetic Resonance Imaging / methods. Pituitary Neoplasms / diagnosis
  • [MeSH-minor] Adult. False Negative Reactions. Female. Humans. Male. Middle Aged. Pituitary ACTH Hypersecretion / pathology. Pituitary Gland / pathology. Retrospective Studies

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  • [Cites] AJR Am J Roentgenol. 1989 Jan;152(1):145-51 [2783269.001]
  • [Cites] J Comput Assist Tomogr. 1988 Sep-Oct;12(5):728-35 [3170830.001]
  • [Cites] Neurosurgery. 1988 Feb;22(2):380-5 [2832783.001]
  • [Cites] AJNR Am J Neuroradiol. 1988 Jan-Feb;9(1):5-11 [3124586.001]
  • [Cites] Radiology. 1987 May;163(2):421-6 [3562821.001]
  • [Cites] Radiology. 1986 Dec;161(3):761-5 [3786729.001]
  • [Cites] Radiol Clin North Am. 1989 Mar;27(2):265-81 [2645603.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Jul;89(7):3371-6 [15240617.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Apr;88(4):1565-9 [12679440.001]
  • [Cites] Clin Endocrinol (Oxf). 1998 Sep;49(3):293-300 [9861318.001]
  • [Cites] J Clin Endocrinol Metab. 1995 Nov;80(11):3114-20 [7593411.001]
  • [Cites] Radiology. 1990 Aug;176(2):419-28 [2164234.001]
  • [Cites] Radiographics. 1989 Jul;9(4):587-98 [2756189.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Aug;89(8):3795-800 [15292307.001]
  • (PMID = 19500112.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 HD008833-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Other-IDs] NLM/ NIHMS139974; NLM/ PMC2866063
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70. Batista DL, Zhang X, Gejman R, Ansell PJ, Zhou Y, Johnson SA, Swearingen B, Hedley-Whyte ET, Stratakis CA, Klibanski A: The effects of SOM230 on cell proliferation and adrenocorticotropin secretion in human corticotroph pituitary adenomas. J Clin Endocrinol Metab; 2006 Nov;91(11):4482-8
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  • [Title] The effects of SOM230 on cell proliferation and adrenocorticotropin secretion in human corticotroph pituitary adenomas.
  • CONTEXT: There is no tumor-directed medical therapy available for Cushing's disease.
  • OBJECTIVE: The objective was to determine the in vitro effect of the somatostatin analog pasireotide (SOM230) on cell proliferation in human corticotroph tumors.
  • DESIGN/METHODS: Expression of somatostatin receptors (SSTR 1-5) was determined by quantitative RT-PCR in 13 human corticotroph tumors and by immunohistochemistry (IHC) in 12 of the 13 tumors.
  • SOM230 effects on cell proliferation and ACTH release were evaluated in vitro using primary cultures of six of the 13 human corticotroph adenomas.
  • RESULTS: In our series, we found expression of SSTR subtypes 1, 2, 4, and 5 in human corticotroph tumors by quantitative RT-PCR.
  • Significant suppression of cell proliferation was observed in all tumors cultured (percent suppression range: 10-70%; P = 0.045-0.001).
  • SOM230 inhibited ACTH secretion in five of the six tumors cultured (percent suppression range: 23-56%; P = 0.042-0.001).
  • CONCLUSION: Corticotroph tumors express multiple SSTR subtypes.
  • SOM230 significantly suppressed cell proliferation and ACTH secretion in primary cultures of human corticotroph tumors.
  • These in vitro results support the hypothesis that SOM230 may have a role in the medical therapy of corticotroph tumors.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / drug therapy. Adenoma / drug therapy. Adrenocorticotropic Hormone / secretion. Cell Proliferation / drug effects. Somatostatin / analogs & derivatives
  • [MeSH-minor] Adolescent. Adult. Child. Female. Humans. Immunohistochemistry. In Vitro Techniques. Male. Middle Aged. Pituitary ACTH Hypersecretion / drug therapy. RNA, Messenger / metabolism. Receptors, Somatostatin / metabolism. Tumor Cells, Cultured

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  • (PMID = 16940446.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Receptors, Somatostatin; 51110-01-1 / Somatostatin; 9002-60-2 / Adrenocorticotropic Hormone; 98H1T17066 / pasireotide
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71. Weil RJ, Vortmeyer AO, Nieman LK, Devroom HL, Wanebo J, Oldfield EH: Surgical remission of pituitary adenomas confined to the neurohypophysis in Cushing's disease. J Clin Endocrinol Metab; 2006 Jul;91(7):2656-64
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Surgical remission of pituitary adenomas confined to the neurohypophysis in Cushing's disease.
  • CONTEXT: Partial or total removal of the pituitary cures 60-80% of patients with Cushing's disease (CD) in whom an adenoma cannot be identified at surgery.
  • Tumor was visible at surgery in 11 patients; all 12 tumors were positive for ACTH by immunohistochemistry.
  • Hypopituitarism or long-term neurohypophysial dysfunction has not occurred.
  • CONCLUSION: We report a new subset of patients with CD, ACTH-secreting adenomas that arise wholly within the posterior lobe of the pituitary gland.
  • In cases of CD in which an adenoma is not identified in the adenohypophysis and in patients with persistent hypercortisolism after complete or partial excision of the anterior lobe, tumor within the neurohypophysis should be considered; selective adenomectomy of a neurohypophyseal, ACTH-secreting tumor can produce long-term remission.
  • [MeSH-major] Adenoma / surgery. Pituitary ACTH Hypersecretion / surgery. Pituitary Gland, Posterior / surgery. Pituitary Neoplasms / surgery

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  • (PMID = 16636117.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
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72. Hofland LJ, van der Hoek J, Feelders R, van der Lely AJ, de Herder W, Lamberts SW: Pre-clinical and clinical experiences with novel somatostatin ligands: advantages, disadvantages and new prospects. J Endocrinol Invest; 2005;28(11 Suppl International):36-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • GH-secreting pituitary adenomas preferentially express SSTR2 and SSTR5, prolactinomas SSTR1 and SSTR5, and corticotroph adenomas express SSTR2 (low number) and predominantly SSTR5s.
  • In patients with GEP neuroendocrine tumors, both somatostatin-analogs effectively suppress the production of bioactive peptides and hormones by the tumor cells, resulting in an important improvement of the related clinical symptomatology.
  • In vitro studies using human pituitary adenoma cells demonstrate a more profound inhibition of GH, PRL and ACTH secretion by somatostatin-analogs targeting both SSTR2s and SSTR5s, compared with SSTR2-preferential somatostatin-analogs.
  • This likely reflects the SSTR subtype expression pattern in the adenoma cells.
  • [MeSH-minor] Acromegaly / drug therapy. Adenoma / drug therapy. Animals. Carcinoma, Neuroendocrine / drug therapy. Endocrine Gland Neoplasms / drug therapy. Gene Expression. Humans. Ligands. Neurosecretory Systems. Pituitary ACTH Hypersecretion / drug therapy. Pituitary Neoplasms / drug therapy. Receptors, Somatostatin / drug effects. Receptors, Somatostatin / genetics. Receptors, Somatostatin / physiology

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  • (PMID = 16625843.001).
  • [ISSN] 0391-4097
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Ligands; 0 / Receptors, Somatostatin; 51110-01-1 / Somatostatin
  • [Number-of-references] 40
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73. Karavitaki N, Scheithauer BW, Watt J, Ansorge O, Moschopoulos M, Llaguno AV, Wass JA: Collision lesions of the sella: co-existence of craniopharyngioma with gonadotroph adenoma and of Rathke's cleft cyst with corticotroph adenoma. Pituitary; 2008;11(3):317-23
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  • [Title] Collision lesions of the sella: co-existence of craniopharyngioma with gonadotroph adenoma and of Rathke's cleft cyst with corticotroph adenoma.
  • Most contributions include a pituitary adenoma or a cyst/cystic tumor, particularly a Rathke cleft cyst.
  • The association of craniopharyngioma with an adenoma is particularly rare.
  • Among reported cases, some have included secondary prolactin cell hyperplasia due to pituitary stalk section effect.
  • Herein, we report two collision lesions, including a gonadotroph adenoma with adamantinomatous craniopharyngioma and a corticotroph adenoma with Rathke's cleft cyst.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / complications. Adenoma / complications. Central Nervous System Cysts / complications. Corticotrophs / pathology. Craniopharyngioma / complications. Gonadotrophs / pathology. Pituitary Neoplasms / complications. Sella Turcica / pathology

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  • [Cites] No Shinkei Geka. 2005 Aug;33(8):797-803 [16095210.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 1986 Nov;49(11):1305-7 [3794737.001]
  • [Cites] No To Shinkei. 1969 Dec;21(12):1326-9 [5395295.001]
  • [Cites] Arch Pathol. 1970 Nov;90(5):444-50 [5476241.001]
  • [Cites] Am J Clin Pathol. 2003 Nov;120(5):732-6 [14608900.001]
  • [Cites] J Clin Invest. 2003 Dec;112(11):1603-18 [14660734.001]
  • [Cites] Oral Surg Oral Med Oral Pathol. 1959 Feb;12(2):199-205 [13633216.001]
  • [Cites] Am J Pathol. 2002 Dec;161(6):1997-2001 [12466115.001]
  • [Cites] Arch Pathol Lab Med. 1994 May;118(5):562-5 [8192565.001]
  • [Cites] Arch Dis Child. 1987 Oct;62(10):1077-8 [2823728.001]
  • [Cites] Endocr Rev. 2006 Jun;27(4):371-97 [16543382.001]
  • [Cites] J Pathol. 2004 Jul;203(3):814-21 [15221941.001]
  • [Cites] JAMA. 1978 Aug 4;240(5):471-3 [660898.001]
  • [Cites] J Neurosurg. 1966 Aug;25(2):199-204 [5296495.001]
  • [Cites] Endocr Rev. 1998 Dec;19(6):798-827 [9861546.001]
  • [Cites] Intern Med J. 2004 Sep-Oct;34(9-10):573-6 [15482272.001]
  • [Cites] Cancer. 1978 Jan;41(1):337-43 [626939.001]
  • [Cites] No Shinkei Geka. 1984 Jun;12(7):833-8 [6483092.001]
  • [Cites] Anat Rec. 1951 Feb;109(2):217-31 [14811058.001]
  • [Cites] Virchows Arch A Pathol Anat Histopathol. 1983;399(1):49-59 [6299000.001]
  • [Cites] Acta Neuropathol. 2005 Jun;109(6):589-97 [15891929.001]
  • [Cites] No Shinkei Geka. 1987 Dec;15(12):1313-8 [3448501.001]
  • [Cites] Mayo Clin Proc. 1989 Sep;64(9):1077-84 [2811485.001]
  • [Cites] No Shinkei Geka. 1986 Mar;14 (3 Suppl):435-40 [3703147.001]
  • [Cites] Endocrinology. 2002 Nov;143(11):4429-36 [12399440.001]
  • [Cites] Neuroradiology. 2001 Sep;43(9):755-9 [11594426.001]
  • [Cites] Endocr Pathol. 2001 Summer;12(2):125-36 [11579678.001]
  • [Cites] J Neurosurg. 2004 Jan;100(1):33-40 [14743909.001]
  • [Cites] Oral Surg Oral Med Oral Pathol. 1983 Nov;56(5):502-11 [6196702.001]
  • [Cites] Surg Neurol. 1989 May;31(5):381-6 [2711312.001]
  • [Cites] J Neurosurg. 2003 Jan;98(1):162-4 [12546365.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 1975 Aug;38(8):782-6 [1185198.001]
  • [Cites] Neurosurgery. 1987 Sep;21(3):371-7 [3670583.001]
  • [Cites] J Neurosurg. 1966 Jan;24(1):77-81 [5903300.001]
  • [Cites] Neurosurgery. 1985 Oct;17(4):657-9 [4058703.001]
  • [Cites] Clin Endocrinol (Oxf). 2005 Apr;62(4):397-409 [15807869.001]
  • [Cites] J Pathol. 1971 Mar;103(3):185-7 [5567175.001]
  • [Cites] Br J Neurosurg. 1995;9(1):51-5 [7786427.001]
  • [Cites] J Neurooncol. 2005 Jul;73(3):205-9 [15980970.001]
  • [Cites] Cancer. 1972 Feb;29(2):423-30 [5013542.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Jul;82(7):2357-62 [9215319.001]
  • [Cites] Pediatr Neurosurg. 1994;21 Suppl 1:2-10 [7841074.001]
  • [Cites] J Neurosurg. 1994 Jun;80(6):1018-25 [8189257.001]
  • [Cites] J Neurosurg. 1998 Oct;89(4):547-51 [9761047.001]
  • [Cites] No Shinkei Geka. 1987 Sep;15(9):999-1003 [3320806.001]
  • [Cites] Zh Vopr Neirokhir Im N N Burdenko. 1981 Nov-Dec;(6):52-4 [7336839.001]
  • [Cites] J Neurosurg. 2005 Apr;102(3 Suppl):318-21 [15881759.001]
  • [Cites] J Pathol Bacteriol. 1955 Jan-Apr;69(1-2):141-5 [13243181.001]
  • [Cites] Arch Pathol. 1960 Sep;70:293-9 [13850582.001]
  • [Cites] Cancer. 1976 Apr;37(4):1944-52 [1260697.001]
  • [Cites] Neurosurgery. 2000 Feb;46(2):291-302; discussion 302-5 [10690718.001]
  • [Cites] Cancer Genet Cytogenet. 1992 Mar;59(1):12-9 [1313329.001]
  • [Cites] Surg Neurol. 1994 Aug;42(2):112-6 [8091286.001]
  • [Cites] Cancer Genet Cytogenet. 1992 Jun;60(2):212-3 [1606570.001]
  • [Cites] Pituitary. 2004;7(1):39-44 [15638297.001]
  • [Cites] Endocr Pathol. 2002 Summer;13(2):157-65 [12165665.001]
  • [Cites] Intern Med. 1997 Feb;36(2):107-12 [9099592.001]
  • [Cites] Acta Neuropathol. 1992;83(2):211-5 [1557952.001]
  • [Cites] J Neurosurg. 1988 Oct;69(4):620-3 [3418397.001]
  • [Cites] Neurosci Lett. 2001 Sep 7;310(1):5-8 [11524144.001]
  • [Cites] Neurol Med Chir (Tokyo). 1993 Sep;33(9):643-50 [7505406.001]
  • (PMID = 17917812.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 65
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74. van Rijn SJ, Grinwis GC, Penning LC, Meij BP: Expression of Ki-67, PCNA, and p27kip1 in canine pituitary corticotroph adenomas. Domest Anim Endocrinol; 2010 May;38(4):244-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of Ki-67, PCNA, and p27kip1 in canine pituitary corticotroph adenomas.
  • Pituitary-dependent hypercortisolism (PDH), which is caused by adrenocorticotropic hormone (ACTH)-secreting pituitary adenomas, is a common endocrinopathy in dogs.
  • The aim of this study was to investigate the expression of the proliferation markers Ki-67 and proliferating cell nuclear antigen (PCNA) and the cell-cycle inhibitor p27kip1 in corticotroph adenomas in enlarged and non-enlarged pituitaries.
  • The expression of Ki-67, PCNA, and p27kip1 was analyzed by immunohistochemical staining of 17 pituitary adenoma samples harvested during pituitary surgery in dogs with PDH.
  • However, a trend toward significance was observed when comparing the expression of p27kip1 in enlarged pituitaries versus normal pituitary tissue.
  • It is concluded that Ki-67 and PCNA are not useful as proliferative markers for studying the pathobiology of pituitary corticotroph adenomas in dogs.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / veterinary. Cyclin-Dependent Kinase Inhibitor p27 / analysis. Dog Diseases / metabolism. Ki-67 Antigen / analysis. Pituitary Neoplasms / veterinary. Proliferating Cell Nuclear Antigen / analysis

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  • [Copyright] Copyright (c) 2009 Elsevier Inc. All rights reserved.
  • (PMID = 20022446.001).
  • [ISSN] 1879-0054
  • [Journal-full-title] Domestic animal endocrinology
  • [ISO-abbreviation] Domest. Anim. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Proliferating Cell Nuclear Antigen; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 581-05-5 / alpha-MSH; 9002-60-2 / Adrenocorticotropic Hormone
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75. Sheehan JM, Douds GL, Hill K, Farace E: Transsphenoidal surgery for pituitary adenoma in elderly patients. Acta Neurochir (Wien); 2008 Jun;150(6):571-4; discussion 574
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transsphenoidal surgery for pituitary adenoma in elderly patients.
  • BACKGROUND: As the population continues to age, the number of elderly patients with symptomatic pituitary tumours will continue to increase.
  • Little information exists as to the safety of pituitary surgery in this patient population.
  • Eight patients had new hormonal deficits post-operatively (1 ACTH, 3 TSH, 2 ACTH/TSH, 2 vasopressin).
  • Surgical removal of pituitary adenomas should be considered the mainstay of treatment in elderly patients in whom treatment is necessary.
  • [MeSH-major] Adenoma / surgery. Endoscopy / methods. Microsurgery / methods. Pituitary Neoplasms / surgery. Postoperative Complications / etiology. Sphenoid Sinus / surgery
  • [MeSH-minor] Age Factors. Aged. Aged, 80 and over. Female. Follow-Up Studies. Growth Hormone-Secreting Pituitary Adenoma / diagnosis. Growth Hormone-Secreting Pituitary Adenoma / surgery. Humans. Image Processing, Computer-Assisted. Magnetic Resonance Imaging. Male. Risk Factors


76. Kalinin PL, Fomichev DV, Kapitanov DN, Kadashev BA, Trunin IuK, Alekseev SN, Kutin MA, Faĭzullaev RB, Gromova VV, Imaev AA: [Rhinological aspects of endoscopic endonasal removal of hypophysial adenomas]. Vestn Otorinolaringol; 2007;(6):10-3
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  • [Title] [Rhinological aspects of endoscopic endonasal removal of hypophysial adenomas].
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / surgery. Endoscopy / methods. Growth Hormone-Secreting Pituitary Adenoma / surgery. Otorhinolaryngologic Surgical Procedures / methods. Sphenoid Bone / surgery

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  • (PMID = 18163085.001).
  • [ISSN] 0042-4668
  • [Journal-full-title] Vestnik otorinolaringologii
  • [ISO-abbreviation] Vestn. Otorinolaringol.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
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77. Gordon BM: Pharmacological management of secreting pituitary tumors. J Neurosci Nurs; 2007 Feb;39(1):52-7
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  • [Title] Pharmacological management of secreting pituitary tumors.
  • Because pituitary adenomas can present in many ways, nurses need to be aware of the signs and symptoms of different hormone-secreting tumors and their related pharmacologic treatment.
  • Although long-term medical management of secreting tumors and their hormonal complications is usually carried out on an outpatient basis, diagnosis often occurs during inpatient care.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / drug therapy. ACTH-Secreting Pituitary Adenoma / nursing. Adenoma / drug therapy. Adenoma / nursing. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / nursing
  • [MeSH-minor] Education, Nursing, Continuing. Growth Hormone-Secreting Pituitary Adenoma / drug therapy. Growth Hormone-Secreting Pituitary Adenoma / nursing. Humans

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  • (PMID = 17396539.001).
  • [ISSN] 0888-0395
  • [Journal-full-title] The Journal of neuroscience nursing : journal of the American Association of Neuroscience Nurses
  • [ISO-abbreviation] J Neurosci Nurs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 12
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78. van der Hoek J, Waaijers M, van Koetsveld PM, Sprij-Mooij D, Feelders RA, Schmid HA, Schoeffter P, Hoyer D, Cervia D, Taylor JE, Culler MD, Lamberts SW, Hofland LJ: Distinct functional properties of native somatostatin receptor subtype 5 compared with subtype 2 in the regulation of ACTH release by corticotroph tumor cells. Am J Physiol Endocrinol Metab; 2005 Aug;289(2):E278-87
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  • [Title] Distinct functional properties of native somatostatin receptor subtype 5 compared with subtype 2 in the regulation of ACTH release by corticotroph tumor cells.
  • In a series of human corticotroph adenomas, we recently found predominant mRNA expression of somatostatin (SS) receptor subtype 5 (sst5).
  • After 72 h, the multiligand SS analog SOM230, which has a very high sst5 binding affinity, but not Octreotide (OCT), significantly inhibited basal ACTH release.
  • To further explore the role of sst5 in the regulation of ACTH release, we conducted additional studies with mouse AtT-20 cells.
  • SOM230 showed a 7-fold higher ligand binding affinity and a 19-fold higher potency in stimulating guanosine 5'-O-(3-thiotriphosphate) binding in AtT-20 cell membranes compared with OCT.
  • SOM230 potently suppressed CRH-induced ACTH release, which was not affected by 48-h dexamethasone (DEX) pretreatment.
  • However, DEX attenuated the inhibitory effects of OCT on ACTH release, whereas it increased the inhibitory potency of BIM-23268, an sst5-specific analog, on ACTH release.
  • Quantitative PCR analysis showed that DEX lowered sst(2A+2B) mRNA expression significantly after 24 and 48 h, whereas sst5 mRNA levels were not significantly affected by DEX treatment.
  • Finally, after SS analog preincubation, compared with OCT both SOM230 and BIM-23268 showed a significantly higher inhibitory effect on CRH-induced ACTH release.
  • In conclusion, our data support the concept that the sst5 receptor might be a target for new therapeutic agents to treat Cushing's disease.
  • [MeSH-major] Adrenocorticotropic Hormone / secretion. Corticotropin-Releasing Hormone / physiology. Pituitary Gland / secretion. Receptors, Somatostatin / physiology
  • [MeSH-minor] Animals. Dose-Response Relationship, Drug. Down-Regulation. Glucocorticoids / physiology. Mice. Octreotide / pharmacology. Pituitary Neoplasms. RNA, Messenger / analysis. Somatostatin / analogs & derivatives. Somatostatin / pharmacology. Stimulation, Chemical. Tumor Cells, Cultured

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  • (PMID = 15769796.001).
  • [ISSN] 0193-1849
  • [Journal-full-title] American journal of physiology. Endocrinology and metabolism
  • [ISO-abbreviation] Am. J. Physiol. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BIM 23268; 0 / Glucocorticoids; 0 / RNA, Messenger; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 0 / somatostatin receptor 5; 51110-01-1 / Somatostatin; 9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone; 98H1T17066 / pasireotide; RWM8CCW8GP / Octreotide
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79. Hoellig A, Niehusmann P, Flacke S, Kristof RA: Metastasis to pituitary adenoma: case report and review of the literature. Cent Eur Neurosurg; 2009 Aug;70(3):149-53
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  • [Title] Metastasis to pituitary adenoma: case report and review of the literature.
  • We present a rare case of a metastasis to a pituitary adenoma and review 14 cases published in the literature to date.
  • Metastases to pituitary adenomas most commonly present with rapidly progressing chiasm compression syndromes, headaches and oculomotor nerve palsies.
  • Metastases to pituitary adenomas have to be considered in the differential diagnosis of sellar tumors.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / pathology. ACTH-Secreting Pituitary Adenoma / secondary. Pituitary Neoplasms / pathology. Pituitary Neoplasms / secondary
  • [MeSH-minor] Aged. Antineoplastic Agents / therapeutic use. Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Fatal Outcome. Humans. Lung Neoplasms / drug therapy. Lung Neoplasms / pathology. Magnetic Resonance Imaging. Male. Neoplasm Metastasis / pathology. Oculomotor Nerve / pathology. Ophthalmoplegia / etiology. Small Cell Lung Carcinoma / pathology. Tomography, X-Ray Computed

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  • [Copyright] Georg Thieme Verlag KG Stuttgart New York.
  • (PMID = 19701874.001).
  • [ISSN] 1868-4912
  • [Journal-full-title] Central European neurosurgery
  • [ISO-abbreviation] Cent Eur Neurosurg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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80. Gruszka A, Kunert-Radek J, Pawlikowski M, Stepien H: Serum endostatin levels are elevated and correlate with serum vascular endothelial growth factor levels in patients with pituitary adenomas. Pituitary; 2005;8(2):163-8
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  • [Title] Serum endostatin levels are elevated and correlate with serum vascular endothelial growth factor levels in patients with pituitary adenomas.
  • The purpose of our study was to evaluate serum concentrations of endostatin in patients harbouring various pituitary adenoma types and to examine the relationship of serum endostatin levels to circulating vascular endothelial growth factor (VEGF) levels.
  • Preoperative serum endostatin and VEGF concentrations were measured using competitive enzyme immunoassays in 71 patients with pituitary adenomas (20 somatotropinomas, 3 corticotropinomas, 6 prolactinomas and 42 clinically nonfunctioning pituitary adenomas - CNFPAs) and compared with levels from age-matched controls.
  • Serum endostatin concentrations were significantly higher in all pituitary adenoma types, except for prolactinomas (somatotropinomas: 124 +/- 16; p < 0.02, corticotropinomas: 157 +/- 42; p < 0.02, prolactinomas: 141 +/- 37; p > 0.05, CNFPAs: 169 +/- 11 ng/ml; p < 0.000005 vs 73 +/- 10 ng/ml in controls).
  • There was a significant positive correlation between endostatin and VEGF serum levels in patients with pituitary adenomas (r = +0.322; p = 0.006).
  • The simultaneous elevation of endostatin and VEGF may attenuate the pro-angiogenic action of VEGF and be responsible for rather weak neovascularization of pituitary adenomas.
  • Prospective studies are required to assess the usefulness of circulating endostatin and VEGF as markers of progression or recurrence of pituitary tumors.
  • [MeSH-major] Adenoma / blood. Endostatins / blood. Pituitary Neoplasms / blood. Vascular Endothelial Growth Factor A / blood

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  • [Cites] Eur J Endocrinol. 2002 Feb;146(2):143-51 [11834422.001]
  • [Cites] J Biol Chem. 1999 Apr 23;274(17):11721-6 [10206987.001]
  • [Cites] Endocr Pathol. 1997 Autumn;8(3):189-193 [12114722.001]
  • [Cites] Nat Med. 1995 Jan;1(1):27-31 [7584949.001]
  • [Cites] J Biol Chem. 2002 Aug 2;277(31):27872-9 [12029087.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Mar;85(3):1159-62 [10720055.001]
  • [Cites] Mediators Inflamm. 2003 Aug;12(4):229-35 [14514474.001]
  • [Cites] Cancer. 2001 Apr 15;91(8):1525-9 [11301401.001]
  • [Cites] Int J Cancer. 1998 Mar 2;75(5):780-6 [9495249.001]
  • [Cites] Neuroendocrinology. 1986;43(2):159-65 [3523276.001]
  • [Cites] EMBO J. 1999 Aug 16;18(16):4414-23 [10449407.001]
  • [Cites] Clin Cancer Res. 2004 Aug 15;10(16):5361-6 [15328173.001]
  • [Cites] Clin Cancer Res. 2000 Dec;6(12):4628-34 [11156212.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Jan;85(1):263-9 [10634397.001]
  • [Cites] Cancer Lett. 2004 Feb 10;204(1):87-95 [14744538.001]
  • [Cites] FEBS Lett. 2000 Dec 15;486(3):247-51 [11119712.001]
  • [Cites] EMBO J. 2000 Mar 15;19(6):1187-94 [10716919.001]
  • [Cites] Urology. 2003 Apr;61(4):719-23 [12670552.001]
  • [Cites] Cell. 1997 Jan 24;88(2):277-85 [9008168.001]
  • [Cites] Cancer Res. 2000 Jan 15;60(2):203-12 [10667560.001]
  • [Cites] J Endocrinol. 1996 Jul;150(1):99-106 [8708569.001]
  • [Cites] Cancer. 2003 Jun 1;97(11):2767-75 [12767089.001]
  • [Cites] J Gastroenterol Hepatol. 2005 Apr;20(4):583-8 [15836707.001]
  • [Cites] Cytobios. 2000;101(398):151-9 [10755214.001]
  • [Cites] Ann Surg Oncol. 2001 Oct;8(9):741-5 [11597016.001]
  • [Cites] Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2004 Apr;26(2):164-7 [15171554.001]
  • [Cites] Clin Cancer Res. 2002 Sep;8(9):2933-8 [12231538.001]
  • [Cites] J Cell Physiol. 1992 Dec;153(3):557-62 [1447317.001]
  • [Cites] Folia Histochem Cytobiol. 2001;39(2):105-6 [11374779.001]
  • [Cites] Endocr Rev. 2003 Oct;24(5):600-32 [14570746.001]
  • [Cites] Cancer Res. 1999 Dec 15;59(24):6052-6 [10626789.001]
  • [Cites] Cancer Res. 2003 Dec 1;63(23):8345-50 [14678995.001]
  • [Cites] Br J Surg. 2004 Oct;91(10):1354-60 [15376182.001]
  • (PMID = 16379029.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Endostatins; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A
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81. Mauermann WJ, Sheehan JP, Chernavvsky DR, Laws ER, Steiner L, Vance ML: Gamma Knife surgery for adrenocorticotropic hormone-producing pituitary adenomas after bilateral adrenalectomy. J Neurosurg; 2007 Jun;106(6):988-93
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  • [Title] Gamma Knife surgery for adrenocorticotropic hormone-producing pituitary adenomas after bilateral adrenalectomy.
  • OBJECT: Patients with adrenocorticotropic hormone (ACTH)-secreting pituitary adenomas may require a bilateral adrenalectomy to treat their Cushing's disease.
  • Approximately one third of these patients, however, will experience progressive enlargement of the residual pituitary adenoma, develop hyperpigmentation, and have an elevated level of serum ACTH.
  • METHODS: The prospectively collected University of Virginia Gamma Knife database of patients with pituitary adenomas was reviewed to identify all individuals with Nelson's syndrome who were treated with GKS.
  • These patients were assessed for tumor control (that is, lack of tumor growth over time) with neuroimaging studies (median follow-up duration 22 months) and for biochemical normalization of their ACTH levels (median follow-up duration 50 months).
  • Neuroimaging follow-up studies were available for 22 patients, and endocrine follow up was available for 15 patients in whom elevation of ACTH levels was documented prior to GKS.
  • In the 22 patients in whom neuroimaging follow-up studies were available, 12 had a decrease in tumor size, eight had no tumor growth, and two had an increase in tumor volume.
  • Ten of 15 patients with elevated ACTH levels prior to GKS showed a decrease in their ACTH levels at last follow up; three of these 10 patients achieved normal ACTH levels (< 50 pg/ml) and the other five patients with initially elevated values had an increase in ACTH levels.
  • Ten patients were thoroughly evaluated for post-GKS pituitary function; four were found to have new pituitary hormone deficiency and six did not have hypopituitarism after GKS.
  • CONCLUSIONS: Gamma Knife surgery may control the residual pituitary adenoma and decrease ACTH levels in patients with Nelson's syndrome.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / surgery. Adrenalectomy. Nelson Syndrome / surgery. Radiosurgery

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  • (PMID = 17564169.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone
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82. Utz A, Biller BM: The role of bilateral inferior petrosal sinus sampling in the diagnosis of Cushing's syndrome. Arq Bras Endocrinol Metabol; 2007 Nov;51(8):1329-38
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  • [Title] The role of bilateral inferior petrosal sinus sampling in the diagnosis of Cushing's syndrome.
  • Adrenocorticotropin hormone (ACTH)-dependent Cushing's syndrome is most often due to a pituitary corticotroph adenoma, with ectopic ACTH-secreting tumors representing approximately 15% of cases.
  • BIPSS is an interventional radiology procedure in which ACTH levels obtained from venous drainage very near the pituitary gland are compared to peripheral blood levels before and after corticotropin hormone (CRH) stimulation.
  • A gradient between these two locations indicates pituitary Cushing's, whereas the absence of a gradient suggests ectopic Cushing's.
  • Accurate BIPSS results require hypercortisolemia to suppress normal corticotroph ACTH production and hypercortisolemia at the time of the BIPSS to assure excessive ACTH secretion.
  • In some cases, intrapituitary gradients from side-to-side can be helpful to localize small corticotroph adenomas within the sella.
  • [MeSH-major] ACTH Syndrome, Ectopic / diagnosis. Cushing Syndrome / diagnosis. Petrosal Sinus Sampling
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / blood. ACTH-Secreting Pituitary Adenoma / diagnosis. ACTH-Secreting Pituitary Adenoma / secretion. Adenoma / blood. Adenoma / diagnosis. Adenoma / secretion. Adrenocorticotropic Hormone / blood. Corticotropin-Releasing Hormone. Diagnosis, Differential. Humans. Pituitary Neoplasms / blood. Pituitary Neoplasms / diagnosis. Pituitary Neoplasms / secretion. Sensitivity and Specificity

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  • (PMID = 18209871.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Brazil
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone
  • [Number-of-references] 37
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83. Rosales C, Fierrard H, Bertagna X, Raffin-Sanson ML: [Management of hypercortisolism]. Rev Med Interne; 2008 Apr;29(4):337-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE: Cushing's syndrome is a rare but frequently considered disease.
  • Its diagnosis can lead to some difficulties, including confirming the effective endogenous hypercortisolism and determining its cause.
  • The severity of this disease, the diversity of its complications and the multiple therapeutic options make its management challenging.
  • The aim of this review is to present the most recent data about management of Cushing's syndrome, especially diagnostic approaches and therapeutic options.
  • MAIN POINTS: We retained the following points: midnight salivary cortisol is a useful tool in the diagnosis of Cushing's syndrome; the desmopressin test can help to distinguish between Cushing's syndrome and "pseudoCushing's" due to alcohol consumption or psychiatric disorders; cavernous sinus and inferior petrosal sinus sampling is indicated in the evaluation of ACTH-dependent Cushing's syndromes when pituitary imaging is normal or equivocal or when dynamic tests are contradictory; multislice computed-tomography of the chest and the abdomen and somatostatin analogue scintigraphy, eventually combined, are the best imaging procedures in occult ectopic ACTH syndromes; patients with Cushing's disease should be referred to a neurosurgeon experienced in corticotroph adenomas surgery; metabolic consequences of Cushing's syndrome, such as cardiovascular risk factors and osteoporosis need an aggressive treatment.
  • PERSPECTIVES: The incidence of Cushing's syndrome is only 1/100000 per year.
  • Endocrinological management of the disease improves metabolic disorders in these patients.
  • If these results are confirmed, screening for Cushing's syndrome should be systematically performed in these populations.

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  • (PMID = 18226430.001).
  • [ISSN] 0248-8663
  • [Journal-full-title] La Revue de medecine interne
  • [ISO-abbreviation] Rev Med Interne
  • [Language] FRE
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Enzyme Inhibitors; 78E4J5IB5J / Mitotane; R9400W927I / Ketoconazole
  • [Number-of-references] 42
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84. van der Klaauw AA, Kienitz T, Strasburger CJ, Smit JW, Romijn JA: Malignant pituitary corticotroph adenomas: report of two cases and a comprehensive review of the literature. Pituitary; 2009;12(1):57-69
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  • [Title] Malignant pituitary corticotroph adenomas: report of two cases and a comprehensive review of the literature.
  • Corticotroph pituitary carcinomas are tumors, defined by the presence of distant metastases that determine their poor prognosis.
  • The diagnosis and therapy of malignant corticotroph adenomas remains a clinical challenge.
  • The molecular mechanisms of malignant transformation of pituitary adenomas are unclear, although they are believed to arise in an adenoma-to-carcinoma sequence.
  • We describe two cases of malignant Cushing's disease with metastases in liver and bone, respectively.
  • The primary pituitary tumors were treated by a combination of radiotherapy and transsphenoidal surgery, but recurred several times in both patients.
  • The time interval between the diagnosis of Cushing's disease and the discovery of metastases was 32 and 17 years, respectively.
  • In the first case the patient died within 6 months after diagnosis of metastasis, whereas the second patient is alive at a follow-up of 2 years after the discovery of the metastasis.
  • Furthermore, we reviewed all available cases of corticotroph pituitary carcinomas reported in the literature and analyzed their clinical features and therapeutical management.
  • In conclusion, frequent relapses of Cushing's disease, aggressive growth of macroadenoma, Nelson's syndrome after adrenalectomy or persistently high ACTH levels should prompt the clinician to consider the possibility of pituitary corticotroph carcinomas.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / diagnosis. ACTH-Secreting Pituitary Adenoma / pathology. Pituitary ACTH Hypersecretion / complications

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  • [Cites] Neurosurgery. 2000 Sep;47(3):723-9; discussion 729-30 [10981760.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Jan;83(1):63-7 [9435417.001]
  • [Cites] Rev Med Interne. 1991 May-Jun;12(3):209-12 [1896714.001]
  • [Cites] Clin Endocrinol (Oxf). 2001 Oct;55(4):549-56 [11678840.001]
  • [Cites] Diagn Imaging Clin Med. 1984;53(6):292-7 [6096073.001]
  • [Cites] Henry Ford Hosp Med J. 1984;32(1):61-6 [6746304.001]
  • [Cites] J Clin Endocrinol Metab. 2007 Jan;92(1):172-9 [17062771.001]
  • [Cites] J Neurosurg. 2002 Feb;96(2):352-60 [11838811.001]
  • [Cites] Endocrinol Jpn. 1992 Apr;39(2):177-84 [1327728.001]
  • [Cites] J Neuropathol Exp Neurol. 1953 Jul;12(3):205-23 [13061969.001]
  • [Cites] Pituitary. 2000 Oct;3(2):105-12 [11141693.001]
  • [Cites] Ann Endocrinol (Paris). 1997;58(6):503-9 [9686010.001]
  • [Cites] Clin Endocrinol (Oxf). 1986 Aug;25(2):117-26 [3024876.001]
  • [Cites] Cancer Lett. 1998 Apr 24;126(2):209-14 [9585068.001]
  • [Cites] Neurosurg Focus. 2004 Apr 15;16(4):E7 [15191336.001]
  • [Cites] Acta Cytol. 2006 Mar-Apr;50(2):225-30 [16610696.001]
  • [Cites] Endocr Rev. 1998 Oct;19(5):647-72 [9793762.001]
  • [Cites] Ann Intern Med. 1976 Dec;85(6):731-4 [999109.001]
  • [Cites] J Clin Endocrinol Metab. 1983 Sep;57(3):649-53 [6308034.001]
  • [Cites] Clin Endocrinol (Oxf). 1995 Jun;42(6):663-70; discussion 671-2 [7634510.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Dec;88(12):5858-64 [14671181.001]
  • [Cites] Cancer. 1997 Feb 15;79(4):804-12 [9024719.001]
  • [Cites] Gen Diagn Pathol. 1995 Oct;141(2):81-92 [8548598.001]
  • [Cites] J Clin Endocrinol Metab. 2005 May;90(5):3089-99 [15741248.001]
  • [Cites] J Pathol Bacteriol. 1947 Jan-Apr;59(1-2):137-44 [20266356.001]
  • [Cites] Clin Endocrinol (Oxf). 2001 May;54(5):617-26 [11380492.001]
  • [Cites] Endocrine. 2005 Oct;28(1):115-21 [16311418.001]
  • [Cites] J Clin Endocrinol Metab. 1990 Oct;71(4):1068-73 [1698198.001]
  • [Cites] Eur J Endocrinol. 2006 Oct;155(4):523-34 [16990651.001]
  • [Cites] Endocr Pathol. 1998 Spring;9(1):53-62 [12114662.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Jul;87(7):3084-9 [12107205.001]
  • [Cites] J Clin Endocrinol Metab. 1995 Jan;80(1):165-71 [7829606.001]
  • [Cites] Arch Pathol. 1975 Jan;99(1):32-5 [1111493.001]
  • [Cites] Ann Intern Med. 1994 May 15;120(10):817-20 [8154641.001]
  • [Cites] Endocr J. 2002 Apr;49(2):153-8 [12081233.001]
  • [Cites] Am J Surg Pathol. 2003 Apr;27(4):477-86 [12657932.001]
  • [Cites] Appl Pathol. 1984;2(1):10-21 [6098287.001]
  • [Cites] Ultrastruct Pathol. 2001 May-Jun;25(3):227-42 [11465479.001]
  • [Cites] J Endocrinol Invest. 1992 May;15(5):387-91 [1324266.001]
  • [Cites] Clin Endocrinol (Oxf). 2005 Nov;63(5):549-59 [16268808.001]
  • [Cites] Dtsch Med Wochenschr. 2004 Feb 13;129(7):310-2 [14765329.001]
  • [Cites] Arch Pathol Lab Med. 1995 Jan;119(1):93-6 [7802565.001]
  • [Cites] Acta Endocrinol (Copenh). 1986 Mar;111(3):300-4 [3008476.001]
  • [Cites] Pituitary. 2003;6(1):41-7 [14674723.001]
  • [Cites] J Endocrinol Invest. 1999 Jan;22(1):70-5 [10090141.001]
  • [Cites] J Clin Endocrinol Metab. 1996 Jul;81(7):2647-52 [8675592.001]
  • [Cites] J Endocrinol Invest. 2002 Jan;25(1):65-72 [11883868.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Sep;79(3):887-9 [8077377.001]
  • [Cites] Dtsch Med Wochenschr. 2000 Jan 21;125(3):52-6 [10681999.001]
  • [Cites] Am J Med. 1954 Jul;17(1):134-42 [13171400.001]
  • [Cites] Cancer. 1996 Aug 1;78(3):502-10 [8697397.001]
  • [Cites] Eur J Endocrinol. 1997 Aug;137(2):176-80 [9272107.001]
  • [Cites] Pathol Res Pract. 1999;195(3):183-7 [10220799.001]
  • [Cites] Clin Endocrinol (Oxf). 2002 Apr;56(4):541-51 [11966748.001]
  • [Cites] J Assoc Physicians India. 2000 Apr;48(4):448-9 [11273189.001]
  • [Cites] Front Horm Res. 2006;34:158-84 [16474220.001]
  • [Cites] J Clin Endocrinol Metab. 1959 Dec;19:1523-39 [14440922.001]
  • [Cites] Endocr Pathol. 2001 Fall;12(3):329-41 [11740054.001]
  • [Cites] J Neurooncol. 2001 Sep;54(2):121-7 [11761429.001]
  • [Cites] J Endocrinol Invest. 1997 Apr;20(4):230-6 [9211132.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Dec;83(12 ):4233-8 [9851756.001]
  • (PMID = 18176844.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 62
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85. Hashiba T, Saitoh Y, Asanuma N, Kouhara H, Maruo T, Fujinaka T, Kasayama S, Yoshimine T: Reduction of a pancreatic tumor after total removal of an ACTH secreting pituitary tumor: differential diagnosis of Cushing's syndrome. Endocr J; 2006 Apr;53(2):203-8
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  • [Title] Reduction of a pancreatic tumor after total removal of an ACTH secreting pituitary tumor: differential diagnosis of Cushing's syndrome.
  • Endocrinologic tests sometimes fail to distinguish adrenocorticotropic hormone (ACTH)-secreting pituitary adenoma from ectopic ACTH-secreting tumor.
  • The authors experienced a case of Cushing's disease associated with a pancreatic tumor.
  • Venous sampling contributed to the final diagnosis of Cushing's disease in this complex case, while endocrinologic tests showed paradoxical results.
  • A 54-year-old woman presented with Cushing's syndrome and pancreatic tumor.
  • Magnetic resonance imaging (MRI) failed to reveal a pituitary tumor, but a gadolinium-enhanced tumor with cystic components was seen in the pancreatic tail.
  • Results of conventional endocrinologic tests suggested ectopic ACTH syndrome, but venous sampling including cavernous sinus sampling indicated an ACTH-secreting pituitary adenoma.
  • Transsphenoidal surgery revealed a pituitary microadenoma, and total removal of the tumor was achieved.
  • Postoperative abdominal MRI revealed that the pancreatic tumor diminished gradually without treatment.
  • Selective cavernous sinus sampling was useful for distinguishing ACTH-secreting pituitary adenoma from ectopic ACTH syndrome in this complex case.
  • This was a rare case in which the pancreatic tumor diminished after total removal of the ACTH-secreting pituitary adenoma.
  • [MeSH-major] Adrenocorticotropic Hormone / secretion. Cushing Syndrome / diagnosis. Pancreatic Neoplasms / complications. Pituitary Neoplasms / secretion
  • [MeSH-minor] ACTH Syndrome, Ectopic / diagnosis. Adenoma / secretion. Adenoma / surgery. Diagnosis, Differential. Female. Follow-Up Studies. Humans. Magnetic Resonance Imaging. Middle Aged. Pituitary ACTH Hypersecretion / diagnosis. Positron-Emission Tomography


86. Kovacs K, Horvath E: Effects of medical therapy on pituitary tumors. Ultrastruct Pathol; 2005 May-Aug;29(3-4):163-7
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  • [Title] Effects of medical therapy on pituitary tumors.
  • Previously surgery and irradiation were the only available procedures to treat patients with pituitary tumors.
  • This paper summarizes the effect of medical therapy on the morphologic features of pituitary tumors and illustrates the ultrastructural alterations on electron micrographs.
  • Currently drugs can be used in the management of pituitary tumors secreting GH, PRL, and/or TSH in excess.
  • No medical therapy is available so far for ACTH-, FSH-, LH-, or alpha-subunit-secreting tumors as well as non-hormone-secreting pituitary tumors.
  • Dopamine agonists are effective in the management of PRL-secreting tumors; they cause marked reversible tumor shrinkage in the substantial majority of patients.
  • Long-acting somatostatin analogs are useful in the management of GH- and TSH-secreting pituitary tumors; they lead to mild to moderate tumor shrinkage in approximately 50% of cases.
  • Recently GH receptor blockers (pegvisomant) were introduced in the treatment of GH-producing pituitary adenomas.
  • To the authors' knowledge the effect of these drugs on the morphology of pituitary tumors has not been revealed so far.
  • [MeSH-major] Dopamine Agonists / therapeutic use. Human Growth Hormone / analogs & derivatives. Octreotide / therapeutic use. Pituitary Neoplasms / drug therapy

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  • (PMID = 16036872.001).
  • [ISSN] 0191-3123
  • [Journal-full-title] Ultrastructural pathology
  • [ISO-abbreviation] Ultrastruct Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / pegvisomant; 12629-01-5 / Human Growth Hormone; 9002-62-4 / Prolactin; 9002-71-5 / Thyrotropin; RWM8CCW8GP / Octreotide
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87. Salehi F, Scheithauer BW, Moyes VJ, Drake WM, Syro LV, Manoranjan B, Sharma S, Horvath E, Kovacs K: Low immunohistochemical expression of MGMT in ACTH secreting pituitary tumors of patients with Nelson syndrome. Endocr Pathol; 2010 Dec;21(4):227-9
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  • [Title] Low immunohistochemical expression of MGMT in ACTH secreting pituitary tumors of patients with Nelson syndrome.
  • The aim of the present study was to assess immunohistochemical expression of MGMT in ACTH-secreting pituitary adenomas of patients with Nelson syndrome.
  • Our material consisted of eight specimens from ACTH-secreting pituitary adenomas of patients with Nelson syndrome.
  • Absent or low MGMT staining in brain and other neoplasms has been shown to correlate with successful treatment with temozolomide, and recent reports of aggressive pituitary adenomas suggest similar outcomes.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / metabolism. Adenoma / metabolism. DNA Modification Methylases / biosynthesis. DNA Repair Enzymes / biosynthesis. Nelson Syndrome / metabolism. Tumor Suppressor Proteins / biosynthesis

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  • [Cites] J Clin Oncol. 2007 Apr 20;25(12 ):1470-5 [17442989.001]
  • [Cites] Clin Endocrinol (Oxf). 2006 Oct;65(4):552-3 [16984254.001]
  • [Cites] Clin Endocrinol (Oxf). 2009 Aug;71(2):226-33 [19067722.001]
  • [Cites] Hormones (Athens). 2009 Oct-Dec;8(4):303-6 [20045804.001]
  • [Cites] Anticancer Agents Med Chem. 2008 May;8(4):368-80 [18473722.001]
  • [Cites] Virchows Arch. 2001 Jun;438(6):595-602 [11469692.001]
  • [Cites] J Clin Oncol. 2006 Jul 20;24(21):3431-7 [16849758.001]
  • [Cites] Hum Pathol. 2007 Jan;38(1):185-9 [17056093.001]
  • [Cites] Acta Neuropathol. 2008 Feb;115(2):261-2 [17926052.001]
  • [Cites] Eur J Endocrinol. 2009 Jan;160(1):115-9 [18984772.001]
  • [Cites] Neurosurgery. 2009 Apr;64(4):E773-4; discussion E774 [19349807.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10 ):997-1003 [15758010.001]
  • [Cites] Neurosurg Focus. 2007;23(3):E13 [17961028.001]
  • [Cites] Jpn J Clin Oncol. 2007 Dec;37(12 ):897-906 [18156172.001]
  • (PMID = 21061089.001).
  • [ISSN] 1559-0097
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Tumor Suppressor Proteins; 7GR28W0FJI / Dacarbazine; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes; YF1K15M17Y / temozolomide
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88. Cavagnini F, Scacchi M, Pecori Giraldi F: Hypopituitarism in Cushing's disease. J Endocrinol Invest; 2008 Sep;31(9 Suppl):44-7
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  • [Title] Hypopituitarism in Cushing's disease.
  • Impaired GH secretion usually accompanies Cushing's syndrome and a variable proportion of patients reportedly fail to recover normal GH secretion after successful treatment.
  • We prospectively studied 34 patients (27 females and 7 males, age range 21- 68 yr) formerly affected by Cushing's disease.
  • All patients had undergone transsphenoidal surgery with the removal of an ACTH-secreting adenoma.
  • Our experience has demonstrated a GHD in a high percentage of patients with Cushing's disease even after long-term remission of hypercortisolism obtained by surgery alone.
  • This finding is significant as it highlights that even the most favorable therapeutical course, i.e. remission achieved by surgery, is often accompanied by impaired GH release.
  • Assessment of GH secretion is therefore recommended in all patients cured from Cushing's disease, even if not submitted to radiotherapy.
  • [MeSH-major] Hypopituitarism / complications. Pituitary ACTH Hypersecretion / complications
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / complications. ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / complications. Adenoma / surgery. Adult. Aged. Female. Follow-Up Studies. Growth Disorders / epidemiology. Growth Disorders / etiology. Human Growth Hormone / blood. Human Growth Hormone / secretion. Humans. Male. Middle Aged. Prevalence. Young Adult

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  • (PMID = 19020385.001).
  • [ISSN] 0391-4097
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone
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89. De Tommasi C, Vance ML, Okonkwo DO, Diallo A, Laws ER Jr: Surgical management of adrenocorticotropic hormone-secreting macroadenomas: outcome and challenges in patients with Cushing's disease or Nelson's syndrome. J Neurosurg; 2005 Nov;103(5):825-30
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  • [Title] Surgical management of adrenocorticotropic hormone-secreting macroadenomas: outcome and challenges in patients with Cushing's disease or Nelson's syndrome.
  • OBJECT: Adrenocorticotropic hormone (ACTH)-secreting pituitary macroadenomas are an uncommon cause of Cushing's disease (CD) and, subsequently, Nelson's syndrome (NS).
  • The outcome of modern surgical treatment is unclear and thus was assessed in a series of 43 patients, with the goal of improving therapeutic results in patients with ACTH-secreting macroadenomas.
  • They represented 15% of the patients surgically treated at the authors' institution for ACTH-secreting adenomas.
  • Remission occurred in 25 (67.6%) of 37 patients with CD, whereas the disease persisted in 12 (32.4%) of 37 patients.
  • After an initial remission, three (12%) of 25 patients demonstrated signs and symptoms indicative of disease recurrence.
  • Invasion of the dura mater by tumor was histologically demonstrated in 10 patients with CD and in two patients with NS.
  • CONCLUSIONS: Comprehensive management of CD caused by ACTH-secreting macroadenomas through the appropriate use of combination therapy, including surgery, radiotherapy, radiosurgery, and adrenalectomy, can lead to outcomes similar to those for microadenomas.
  • Disease recurrence and persistence rates are higher, often because of the invasiveness associated with macroadenomas.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / surgery. Adenoma / surgery. Nelson Syndrome / surgery. Pituitary ACTH Hypersecretion / surgery


90. Fernandez A, Karavitaki N, Wass JA: Prevalence of pituitary adenomas: a community-based, cross-sectional study in Banbury (Oxfordshire, UK). Clin Endocrinol (Oxf); 2010 Mar;72(3):377-82
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  • [Title] Prevalence of pituitary adenomas: a community-based, cross-sectional study in Banbury (Oxfordshire, UK).
  • BACKGROUND: Pituitary adenomas (PAs) are associated with increased morbidity and mortality.
  • All cases of PAs were found following an exhaustive computer database search of agreed terms by the staff of each Practice and data on age, gender, presenting manifestations and their duration, imaging features at diagnosis, history of multiple endocrine neoplasia type 1 and family history of PA were collected.
  • RESULTS: A total of 63 patients with PA were identified amongst the study population of 81,149, with a prevalence of 77.6 PA cases/100,000 inhabitants (prolactinomas; PRLoma: 44.4, nonfunctioning PAs: 22.2, acromegaly; ACRO: 8.6, corticotroph adenoma: 1.2 and unknown functional status; UFS: 1.2/100,000 inhabitants).
  • The distribution of each PA subtype was for PRLoma 57%, nonfunctioning PAs 28%, ACRO 11%, corticotroph adenoma 2% and UFS 2%.
  • The median age at diagnosis and the duration of symptoms until diagnosis (in years) were for PRLoma 32.0 and 1.5, nonfunctioning PAs 51.5 and 0.8, ACRO 47 and 4.5 and corticotroph adenoma 57 and 7, respectively.
  • Five patients (7.9%) presented with classical pituitary apoplexy, with a prevalence of 6.2 cases/100,000 inhabitants.
  • [MeSH-major] Adenoma / epidemiology. Pituitary Neoplasms / epidemiology
  • [MeSH-minor] Adolescent. Adult. Aged. Cross-Sectional Studies. Delayed Diagnosis. England / epidemiology. Female. Humans. Male. Middle Aged. Prevalence. Young Adult

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  • [CommentIn] Clin Endocrinol (Oxf). 2010 Mar;72(3):290-1 [19832856.001]
  • (PMID = 19650784.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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91. Manetti L, Bogazzi F, Giovannetti C, Raffaelli V, Genovesi M, Pellegrini G, Ruocco L, Iannelli A, Martino E: Changes in coagulation indexes and occurrence of venous thromboembolism in patients with Cushing's syndrome: results from a prospective study before and after surgery. Eur J Endocrinol; 2010 Nov;163(5):783-91
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  • [Title] Changes in coagulation indexes and occurrence of venous thromboembolism in patients with Cushing's syndrome: results from a prospective study before and after surgery.
  • OBJECTIVES: To evaluate whether patients with Cushing's syndrome (CS) had i) changes in coagulative and fibrinolytic parameters associated with CS activity and ii) higher prevalence of venous thromboembolic events (VTE).
  • DESIGN: Prospective study conducted on patients with CS evaluated at diagnosis and 12 months after surgery.
  • PATIENTS AND METHODS: Forty patients with active CS (36 with Cushing's disease (CD) and 4 with an adrenal adenoma) were evaluated.
  • Forty normal subjects and 70 patients with non-ACTH-secreting pituitary adenomas served as controls.
  • Patients with still active disease after surgery had higher coagulative parameters than those in remission (VWF (P<0.0001), PAI-1 (P=0.004), TAT (P=0.0001), ATIII (P=0.0002) and α(2) antiplasmin (or SERPINF2; P=0.006)), whereas aPTT levels (P=0.007) were significantly reduced.
  • VTE occurred in three patients with CD (7.5%): one had a pulmonary embolism and two patients had a deep venous thrombosis; no patients submitted to transsphenoidal surgery for non-Cushing's pituitary adenoma had VTE (P=0.04).
  • Thromboprophylaxis seems to be appropriated in patients with active disease, particularly in the postoperative period.


92. Raica M, Coculescu M, Cimpean AM, Ribatti D: Endocrine gland derived-VEGF is down-regulated in human pituitary adenoma. Anticancer Res; 2010 Oct;30(10):3981-6
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  • [Title] Endocrine gland derived-VEGF is down-regulated in human pituitary adenoma.
  • BACKGROUND: Endocrine gland-derived vascular endothelial growth factor (EG-VEGF) is an angiogenic molecule restricted to endocrine glands and, particularly, to steroid-secreting cells.
  • MATERIALS AND METHODS: In this study, we investigated by immunohistochemistry the expression of EG-VEGF in 2 samples of normal adenohypophysis and 43 bioptic samples of pituitary adenoma.
  • Moreover, the expression of growth hormone (GH), prolactin (PRL), follicle-stimulating hormone (FSH), luteinizing hormone (LH), thyroid-stimulating hormone (TSH) and adrenocorticoprophic hormone (ACTH) were also estimated.
  • RESULTS: The results of this study for the first time demonstrate a down-regulation of EG-VEGF expression in human pituitary adenoma as compared to normal adenohypophysis, suggesting an impaired function of the neoplastic cells in terms of hormone release in the blood stream, as a consequence of impaired tumor angiogenesis in the tumor.
  • CONCLUSION: On the basis of our data showing a marked decrease in the expression of EG-VEGF in pituitary adenoma, with the exception of LH-secreting adenomas, we suggest that LH might be involved in the induction of EG-VEGF secretion.
  • [MeSH-major] Adenoma / metabolism. Pituitary Neoplasms / metabolism. Vascular Endothelial Growth Factor, Endocrine-Gland-Derived / biosynthesis
  • [MeSH-minor] Adrenocorticotropic Hormone / biosynthesis. Down-Regulation. Follicle Stimulating Hormone / biosynthesis. Human Growth Hormone / biosynthesis. Humans. Immunohistochemistry. Luteinizing Hormone / biosynthesis. Pituitary Gland, Anterior / metabolism. Prolactin / biosynthesis. Thyrotropin / biosynthesis

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  • (PMID = 21036711.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Vascular Endothelial Growth Factor, Endocrine-Gland-Derived; 12629-01-5 / Human Growth Hormone; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin; 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone; 9002-71-5 / Thyrotropin
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93. Barahona MJ, Sojo L, Wägner AM, Bartumeus F, Oliver B, Cano P, Webb SM: Determinants of neurosurgical outcome in pituitary tumors. J Endocrinol Invest; 2005 Oct;28(9):787-94
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  • [Title] Determinants of neurosurgical outcome in pituitary tumors.
  • OBJECTIVE: Neurosurgery is one of the main therapies for pituitary tumors; optimising outcome is highly desirable for the patient and the health system.
  • We have analysed predictors of outcome in surgically treated pituitary adenomas operated in this centre.
  • DESIGN AND PATIENTS: A total of 289 patients underwent neurosurgery for a pituitary tumor, by the same two neurosurgeons, between 1982 and 2001.
  • Most tumors (70.2%) were macroadenomas; 28.4% were non-functioning, 27.3% secreted PRL, 26.3% GH of which 14 (4.8%) also secreted PRL, 17.3% ACTH, 0.3% FSH and 0.3% TSH.
  • RESULTS: A stepwise, forward logistic regression analysis revealed tumor size as the only significant predictor of radiological cure [odds ratio (OR) for macroadenoma 0.16 vs microadenoma, p=0.0005].
  • Hormonally, PRL-secretion by the tumor was a predictor of poor prognosis (OR 3.29 for cure of non-PRL-secreting tumors, p=0.005), as was tumor size (OR 0.45 for cure of macroadenomas, p=0.005).
  • Considering simultaneous radiological and hormonal remission, tumor size (OR 0.35 for macroadenoma, p=0.0002), and operation date (OR 0.40 for up to 1991, p=0.0002) were the only significant predictors.
  • CONCLUSIONS: PRL secretion, tumor size and operation date are the main predictors of neurosurgical outcome in pituitary tumors, the latter suggesting that neurosurgical experience plays an important role.
  • [MeSH-major] Adenoma / surgery. Neurosurgical Procedures / methods. Pituitary Neoplasms / surgery

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  • [Cites] J Clin Endocrinol Metab. 1998 Oct;83(10):3419-26 [9768641.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Aug;88(8):3567-72 [12915637.001]
  • [Cites] Pituitary. 1999 Jun;2(1):51-4 [11081172.001]
  • [Cites] J Neurosurg. 2004 Apr;100(4):634-8 [15070117.001]
  • [Cites] Eur J Endocrinol. 2002 Feb;146(2):179-86 [11834426.001]
  • [Cites] Clin Endocrinol (Oxf). 2003 Jun;58(6):763-9 [12780754.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Oct;84(10):3696-700 [10523016.001]
  • [Cites] QJM. 1999 Dec;92(12):741-5 [10581337.001]
  • [Cites] Clin Endocrinol (Oxf). 1995 Nov;43(5):517-22 [8548933.001]
  • [Cites] J Neurosurg. 2002 Aug;97(2):307-14 [12186458.001]
  • [Cites] Surg Neurol. 2000 Mar;53(3):211-9 [10773251.001]
  • [Cites] QJM. 1994 Oct;87(10 ):617-23 [7987657.001]
  • [Cites] Clin Endocrinol (Oxf). 1996 Jun;44(6):711-6 [8759184.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Dec;86(12):5695-9 [11739423.001]
  • [Cites] Clin Endocrinol (Oxf). 2003 Jan;58(1):86-91 [12519417.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Oct;83(10):3411-8 [9768640.001]
  • [Cites] BMJ. 1999 Sep 4;319(7210):588-9 [10473459.001]
  • [Cites] Clin Endocrinol (Oxf). 2001 May;54(5):617-26 [11380492.001]
  • [Cites] Clin Endocrinol (Oxf). 1993 Jan;38(1):73-8 [8435888.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Mar;89(3):1131-9 [15001598.001]
  • [Cites] Clin Endocrinol (Oxf). 1996 Sep;45(3):291-8 [8949566.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Apr;86(4):1645-52 [11297598.001]
  • [Cites] BMJ. 1994 Nov 26;309(6966):1409-10 [7819849.001]
  • [Cites] J Endocrinol Invest. 2005 Jan;28(1):18-22 [15816366.001]
  • [Cites] J Neurosurg. 1998 Sep;89(3):353-8 [9724106.001]
  • [Cites] Clin Endocrinol (Oxf). 1999 May;50(5):561-7 [10468920.001]
  • [Cites] Ann Intern Med. 1999 May 18;130(10):821-4 [10366371.001]
  • [Cites] Clin Endocrinol (Oxf). 1999 Sep;51(3):281-4 [10469006.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Dec;85(12):4596-602 [11134114.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Oct;88(10):4709-19 [14557445.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Feb;85(2):526-9 [10690849.001]
  • [Cites] Clin Endocrinol (Oxf). 1992 May;36(5):459-65 [1617796.001]
  • [Cites] J Clin Endocrinol Metab. 1996 Jul;81(7):2647-52 [8675592.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Sep;87(9):4054-8 [12213843.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Jun;89(6):2789-96 [15181059.001]
  • [Cites] Eur J Endocrinol. 2004 Oct;151(4):439-46 [15476442.001]
  • [Cites] Neurosurgery. 1999 Feb;44(2):254-61; discussion 261-3 [9932878.001]
  • [Cites] Clin Endocrinol (Oxf). 2002 Apr;56(4):541-51 [11966748.001]
  • [Cites] Clin Endocrinol (Oxf). 2002 Jan;56(1):25-31 [11849243.001]
  • [Cites] Surg Neurol. 1996 Apr;45(4):341-6 [8607082.001]
  • [Cites] Endocrinol Metab Clin North Am. 1992 Sep;21(3):669-92 [1521518.001]
  • [Cites] Eur J Endocrinol. 1999 Jan;140(1):43-7 [10037250.001]
  • [Cites] Clin Endocrinol (Oxf). 1998 Nov;49(5):653-7 [10197082.001]
  • [Cites] Clin Endocrinol (Oxf). 1996 Oct;45(4):407-13 [8959078.001]
  • (PMID = 16370556.001).
  • [ISSN] 0391-4097
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone; 9002-60-2 / Adrenocorticotropic Hormone
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94. Bush ZM, Lopes MB, Hussaini IM, Jane JA Jr, Laws ER Jr, Vance ML: Immunohistochemistry of COUP-TFI: an adjuvant diagnostic tool for the identification of corticotroph microadenomas. Pituitary; 2010;13(1):1-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunohistochemistry of COUP-TFI: an adjuvant diagnostic tool for the identification of corticotroph microadenomas.
  • Cushing's disease is caused by an ACTH-producing pituitary tumor, and accounts for 10-15% of pituitary tumors.
  • The majority of corticotroph tumors are microadenomas (<10 mm), and accurate histologic identification of these tumors can be challenging because of their small size and the presence of nests of normal corticotroph cells in the anterior pituitary.
  • Retinoic acid has been shown to inhibit ACTH production and induce apoptosis in corticotroph tumor cells.
  • The expression of the orphan nuclear receptor COUP-TFI antagonizes retinoic acid signaling and has been shown to be expressed in normal corticotroph cells, but absent in corticotroph tumor cell lines.
  • We analyzed 34 corticotroph tumor specimens by immunohistochemistry using a goat polyclonal IgG antibody with epitope mapping to the N-terminus of human COUP-TFI.
  • Segments of normal pituitary in each of the 34 specimens demonstrate COUP-TFI immunoreactivity in normal corticotroph cells.
  • Twenty-nine of 34 ACTH producing tumors were immunonegative for COUP-TFI.
  • Two tumors, measuring 9 and 11 mm, showed consistent (>90%) expression of COUP-TFI, and three adenomas (5, 11, and 18 mm) showed heterogenous (20-80%) expression of COUP-TFI.
  • Immunohistochemistry of COUP-TFI may be a useful adjuvant diagnostic tool in distinguishing corticotroph microadenomas from nests of normal corticotroph cells in the anterior pituitary.
  • Furthermore, this study identifies two unique corticotroph tumor populations which differ in their expression of COUP-TFI, the presence of which occurs more frequently in macroadenomas.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / diagnosis. Adenoma / diagnosis. COUP Transcription Factor I / analysis
  • [MeSH-minor] Diagnosis, Differential. Humans. Immunohistochemistry. Molecular Diagnostic Techniques. Retrospective Studies. Tissue Distribution

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  • [Cites] J Clin Invest. 2003 Dec;112(11):1603-18 [14660734.001]
  • [Cites] Endocr Relat Cancer. 2003 Jun;10(2):323-30 [12790793.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Oct;91(10):3746-53 [16868050.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Aug;83(8):2681-6 [9709931.001]
  • [Cites] Cell. 1995 Dec 15;83(6):841-50 [8521508.001]
  • [Cites] Endocr Rev. 1999 Apr;20(2):136-55 [10204115.001]
  • [Cites] Exp Cell Res. 2000 May 1;256(2):545-54 [10772826.001]
  • [Cites] Clin Endocrinol (Oxf). 1999 Jul;51(1):67-71 [10468967.001]
  • [Cites] Endocr Rev. 1998 Oct;19(5):647-72 [9793762.001]
  • [Cites] J Clin Endocrinol Metab. 1990 Dec;71(6):1427-33 [1977759.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Feb;93(2):358-62 [18056770.001]
  • [Cites] Anal Biochem. 1985 Oct;150(1):76-85 [3843705.001]
  • [Cites] Mol Cell Biol. 1995 Feb;15(2):1034-48 [7823919.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Dec;88(12):5593-602 [14671138.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Feb 15;89(4):1448-52 [1311101.001]
  • [Cites] J Clin Invest. 2001 Oct;108(8):1123-31 [11602619.001]
  • [Cites] Clin Genet. 2007 Sep;72(3):175-82 [17718852.001]
  • [Cites] Nat Clin Pract Endocrinol Metab. 2005 Nov;1(1):2-3 [16929356.001]
  • [Cites] J Am Coll Surg. 2001 Dec;193(6):651-9 [11768682.001]
  • [Cites] Neurosurgery. 2000 Mar;46(3):553-8; discussion 558-9 [10719850.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Jan 1;90(1):30-4 [8380496.001]
  • [Cites] Lancet. 2006 May 13;367(9522):1605-17 [16698415.001]
  • [Cites] Endocrinology. 2006 Sep;147(9):4438-44 [16740975.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Feb;84(2):440-8 [10022398.001]
  • [Cites] J Pathol. 1994 Aug;173(4):371-9 [7965396.001]
  • [Cites] Stain Technol. 1974 May;49(3):153-5 [4135794.001]
  • [Cites] J Neurosurg. 1989 Oct;71(4):520-7 [2552045.001]
  • [Cites] J Clin Endocrinol Metab. 1995 Nov;80(11):3114-20 [7593411.001]
  • [Cites] Cell Mol Life Sci. 2000 Sep;57(10):1388-98 [11078018.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Dec;88(12):5808-13 [14671173.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Oct;87(10):4515-21 [12364428.001]
  • [Cites] Am J Clin Pathol. 1981 Jun;75(6):816-21 [6167159.001]
  • [Cites] Endocrinol Metab Clin North Am. 1999 Mar;28(1):211-22 [10207692.001]
  • [Cites] J Neurooncol. 2001 Sep;54(2):121-7 [11761429.001]
  • [Cites] J Steroid Biochem Mol Biol. 1994 Jun;49(4-6):261-7 [8043488.001]
  • (PMID = 19526345.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / 1-T32-DK-07646; United States / NIDDK NIH HHS / DK / T32 DK007646; United States / NCRR NIH HHS / RR / M01RR000847; United States / NIDDK NIH HHS / DK / 1-F32-DK082159-01; United States / NINDS NIH HHS / NS / 5R01NS035122-10
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / COUP Transcription Factor I
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95. Buurman H, Saeger W: Subclinical adenomas in postmortem pituitaries: classification and correlations to clinical data. Eur J Endocrinol; 2006 May;154(5):753-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Subclinical adenomas in postmortem pituitaries: classification and correlations to clinical data.
  • OBJECTIVE: The aim of this study was to examine pituitary adenomas in a series of postmortem pituitaries by use of modern technologies of immunostaining, to classify the adenomas according to the current WHO classification and to analyse the possible associations to the available clinical data.
  • RESULTS: A total of 334 pituitary adenomas were found in 316 pituitaries.
  • One hundred and thirty-two sparsely granulated prolactin cell adenomas (39.5%), 75 null cell adenomas (22.5%) and 31 oncocytomas were diagnosed.
  • Forty-six ACTH cell adenomas (13.8%, 27 densely granulated, 19 sparsely granulated) and one adenoma composed of Crooke's cells were detected.
  • Twenty-two gonadotroph cell adenomas (6.6%), seven GH cell adenomas (four sparsely granulated, three densely granulated), one mixed GH cell-PRL cell adenoma, two TSH cell adenomas, five plurihormonal adenoma type I, four plurihormonal adenoma type II and two alpha-subunit-only adenomas were seen.
  • Six adenomas remained unclassified because the tissue was not contained in all sections for immunohistochemistry.
  • Among 76 adenomas (22.7%), which had a tumour size of > or = 3 mm, only three tumours were macroadenomas corresponding to a tumour size of more than 10 mm.
  • CONCLUSIONS: Adenomas in postmortem pituitaries differ from those in surgical series in proportion of adenoma types and biological behaviour.

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  • (PMID = 16645024.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Glycoprotein Hormones, alpha Subunit; 0 / Gonadotropins; 12629-01-5 / Human Growth Hormone; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin; 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone; 9002-71-5 / Thyrotropin
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96. Trapani F, Del Basso De Caro ML, Insabato L, Papparella S, Paciello O: Type II muscle fibers atrophy associated with silent corticotroph adenoma in a dog. Folia Histochem Cytobiol; 2010 Sep 30;48(3):403-6
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  • [Title] Type II muscle fibers atrophy associated with silent corticotroph adenoma in a dog.
  • The Silent Corticotroph Adenoma (SCA) is a pituitary adenoma variant characterized by the immunoreactivity for adrenocorticotropic hormone (ACTH) and related peptides, without the clinical signs of Cushing's disease.
  • SCA has been postulated to either secrete structurally abnormal ACTH that is inactive but detectable by immunohistochemistry or radioimmunoassay, or to secrete ACTH intermittently or at low levels continuously.
  • Excess of ACTH has been associated to type II muscle atrophy.
  • We describe a case of type II muscle fibers atrophy associated with silent corticotroph adenoma in a dog.
  • The tumour showed a trabecular growth pattern and immunohistochemical analysis demonstrated the presence of cytoplasmic immunoreactivity for ACTH.
  • The muscle atrophy was considered to be related to an excess of inactive ACTH.

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  • (PMID = 21071346.001).
  • [ISSN] 1897-5631
  • [Journal-full-title] Folia histochemica et cytobiologica
  • [ISO-abbreviation] Folia Histochem. Cytobiol.
  • [Language] ENG
  • [Publication-type] Case Reports; Comparative Study; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; EC 1.3.99.1 / Succinate Dehydrogenase; EC 1.6.- / NADH Tetrazolium Reductase
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97. Choe JH, Lee KS, Jeun SS, Cho JH, Hong YK: Endocrine outcome of endoscopic endonasal transsphenoidal surgery in functioning pituitary adenomas. J Korean Neurosurg Soc; 2008 Sep;44(3):151-5
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  • [Title] Endocrine outcome of endoscopic endonasal transsphenoidal surgery in functioning pituitary adenomas.
  • OBJECTIVE: Microscopic and endoscopic transsphenoidal approach (TSA) are major surgical techniques in the treatment of pituitary adenoma.
  • Endoscopic endonasal transsphenoidal approach (EETSA) has been increasingly used for pituitary adenomas, however, its surgical outcome particularly in functioning pituitary adenoma has been debated.
  • Here, we investigated the endocrine outcome of the patients with growth hormone (GH) and adrenocorticotropic hormone (ACTH) secreting pituitary adenoma treated by EETSA.
  • METHODS: We treated 80 patients with pituitary adenoma by EETSA since 2004, of which 12 patients were affected by functioning pituitary adenomas (9 GH, 3 ACTH, 0 PRL; 9 macro, 3 micro).
  • Surgical outcome of those patients treated by EETSA was compared with that of the 11 functioning pituitary adenoma patients (8 GH, 3 ACTH; 8 macro, 3 micro) who underwent sublabial microscopic TSA between 1997 and 2003.
  • CONCLUSION: EETSA appears to be an effective and safe method for the treatment of functioning pituitary adenomas.

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  • [Cites] Am J Rhinol. 2007 Jul-Aug;21(4):510-4 [17882925.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Apr;86(4):1645-52 [11297598.001]
  • [Cites] Am J Rhinol. 2007 Mar-Apr;21(2):203-6 [17424881.001]
  • [Cites] Neuroendocrinology. 2006;83(3-4):240-8 [17047389.001]
  • [Cites] Neurosurgery. 2005 Jun;56(6):1222-33; discussion 1233 [15918938.001]
  • [Cites] Eur J Endocrinol. 2005 Mar;152(3):379-87 [15757854.001]
  • [Cites] Surg Neurol. 1997 Mar;47(3):213-22; discussion 222-3 [9068690.001]
  • [Cites] Neurosurgery. 1996 Jul;39(1):189-92; discussion 192-3 [8805160.001]
  • [Cites] J Laryngol Otol. 1994 Jan;108(1):19-22 [8133158.001]
  • [Cites] Laryngoscope. 1992 Feb;102(2):198-202 [1738293.001]
  • [Cites] J Clin Endocrinol Metab. 1988 May;66(5):1056-64 [3360898.001]
  • [Cites] Neurosurgery. 1987 Aug;21(2):218-22 [2821447.001]
  • [Cites] Clin Neurosurg. 1969;16:185-217 [5811707.001]
  • [Cites] Surg Neurol. 2002 Dec;58(6):371-5; discussion 375-6 [12517610.001]
  • [Cites] J Neurooncol. 2001 Sep;54(2):187-95 [11761435.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Sep;86(9):4072-7 [11549628.001]
  • [Cites] Laryngoscope. 2007 Aug;117(8):1329-32 [17597634.001]
  • (PMID = 19096666.001).
  • [ISSN] 2005-3711
  • [Journal-full-title] Journal of Korean Neurosurgical Society
  • [ISO-abbreviation] J Korean Neurosurg Soc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2588303
  • [Keywords] NOTNLM ; ACTH-secreting pituitary adenoma / Endoscopy / GH-secreting pituitary adenoma / Transsphenoidal approach
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98. La Rosa S, Uccella S, Dainese L, Marchet S, Placidi C, Vigetti D, Capella C: Characterization of c-kit (CD117) expression in human normal pituitary cells and pituitary adenomas. Endocr Pathol; 2008;19(2):104-11
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  • [Title] Characterization of c-kit (CD117) expression in human normal pituitary cells and pituitary adenomas.
  • In experimental animal models, c-kit has been detected in the pars intermedia of the normal pituitary gland and in alpha-melanocyte-stimulating-hormone-positive adenomas and it has been suggested that it plays a role in regulating adrenocorticotropic hormone (ACTH) secretion.
  • To the best of our knowledge, the expression of c-kit in normal human pituitary cells and in pituitary adenomas has never been reported, so the possible biological role of this receptor in the control of pituitary hormone secretion remains unclear.
  • The aim of this study was to evaluate the immunohistochemical expression of c-kit in normal human pituitary glands and in a series of 62 well-characterized pituitary adenomas.
  • Double label immunostaining procedures showed that the c-kit-IR cells corresponded to ACTH cells.
  • Out of 62 adenomas, 15 (24%) were c-kit-IR, including 7/16 (44%) ACTH cell, 3/7 (42%) null cell, 4/11 (36%) alpha-subunit cell, and 1/11 (10%) follicle-stimulating hormone-luteinizing hormone cell adenomas.
  • By contrast, all ten prolactin cell and seven growth hormone cell adenomas were c-kit negative.
  • These data suggest that, in normal conditions, c-kit may be involved in the pituitary-adrenal axis regulation.
  • [MeSH-major] Adenoma / metabolism. Pituitary Gland / metabolism. Pituitary Neoplasms / metabolism. Proto-Oncogene Proteins c-kit / biosynthesis
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / metabolism. ACTH-Secreting Pituitary Adenoma / pathology. Adolescent. Adult. Aged. Blotting, Western. Child. Female. Follicle Stimulating Hormone / blood. Growth Hormone-Secreting Pituitary Adenoma / metabolism. Growth Hormone-Secreting Pituitary Adenoma / pathology. Humans. Immunohistochemistry. Luteinizing Hormone / blood. Male. Middle Aged. Paraffin Embedding. Prolactinoma / metabolism. Prolactinoma / pathology. Tissue Fixation

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  • [Cites] J Histochem Cytochem. 1995 Jan;43(1):97-102 [7822770.001]
  • [Cites] Br J Dermatol. 2004 Feb;150(2):384-5 [14996126.001]
  • [Cites] Cancer Res. 1992 Nov 15;52(22):6139-43 [1384954.001]
  • [Cites] Hum Pathol. 2003 Jan;34(1):18-27 [12605362.001]
  • [Cites] J Histochem Cytochem. 1981 Apr;29(4):577-80 [6166661.001]
  • [Cites] Endocrinology. 2005 Sep;146(9):3985-98 [15932930.001]
  • [Cites] N Engl J Med. 2002 Aug 15;347(7):472-80 [12181401.001]
  • [Cites] Blood. 1999 Sep 15;94(6):1979-86 [10477727.001]
  • [Cites] Appl Immunohistochem Mol Morphol. 2001 Dec;9(4):319-28 [11759058.001]
  • [Cites] EMBO J. 1987 Nov;6(11):3341-51 [2448137.001]
  • [Cites] Ann Oncol. 2003 Jun;14(6):894-7 [12796027.001]
  • [Cites] J Histochem Cytochem. 1994 Nov;42(11):1417-25 [7523489.001]
  • [Cites] Endocr Pathol. 2000 Winter;11(4):315-329 [12114756.001]
  • [Cites] Jpn J Clin Oncol. 2006 Aug;36(8):494-8 [16844734.001]
  • [Cites] Virchows Arch. 2000 Sep;437(3):264-9 [11037346.001]
  • [Cites] Oncogene. 1997 Jun 5;14(22):2661-70 [9178764.001]
  • [Cites] Zentralbl Pathol. 1993 Jun;139(2):165-70 [8396420.001]
  • [Cites] J Clin Endocrinol Metab. 1995 Nov;80(11):3361-7 [7593452.001]
  • [Cites] Hum Pathol. 1998 May;29(5):498-504 [9596274.001]
  • [Cites] Development. 1996 Oct;122(10):3023-33 [8898216.001]
  • [Cites] Mod Pathol. 1998 Aug;11(8):728-34 [9720500.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Dec 23;338(3):1307-15 [16226710.001]
  • [Cites] Mod Pathol. 2005 Mar;18(3):320-3 [15502806.001]
  • [Cites] Neuroendocrinology. 2007;85(2):110-30 [17337880.001]
  • [Cites] Mod Pathol. 2000 Oct;13(10):1134-42 [11048809.001]
  • [Cites] Pathol Int. 1994 Sep;44(9):697-703 [7804432.001]
  • [Cites] Appl Immunohistochem Mol Morphol. 2005 Sep;13(3):205-20 [16082245.001]
  • [Cites] Am J Dermatopathol. 2002 Aug;24(4):289-93 [12142606.001]
  • [Cites] Am J Pathol. 1993 Jan;142(1):339-46 [7678721.001]
  • [Cites] Clin Cancer Res. 2003 Apr;9(4):1469-73 [12684421.001]
  • [Cites] Am J Surg Pathol. 2003 Dec;27(12):1551-8 [14657715.001]
  • [Cites] J Neurosci. 1998 Feb 1;18(3):1056-71 [9437026.001]
  • [Cites] Virchows Arch. 1994;424(2):135-41 [7514077.001]
  • [Cites] J Cutan Pathol. 2004 Mar;31(3):254-61 [14984578.001]
  • [Cites] Stem Cells. 2005;23(1):16-43 [15625120.001]
  • [Cites] Endocr Relat Cancer. 2006 Jun;13(2):535-40 [16728580.001]
  • [Cites] J Neuroimmunol. 1996 Apr;65(2):133-41 [8964895.001]
  • [Cites] Am J Dermatopathol. 2004 Dec;26(6):458-62 [15618926.001]
  • (PMID = 18568298.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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99. Pecori Giraldi F, Bucciarelli LG, Saccani A, Scacchi M, Pesce S, Losa M, Cavagnini F: Ghrelin stimulates adrenocorticotrophic hormone (ACTH) secretion by human ACTH-secreting pituitary adenomas in vitro. J Neuroendocrinol; 2007 Mar;19(3):208-12
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  • [Title] Ghrelin stimulates adrenocorticotrophic hormone (ACTH) secretion by human ACTH-secreting pituitary adenomas in vitro.
  • Ghrelin is a brain-gut peptide with wide-ranging endocrine, metabolic, cardiovascular and neural effects.
  • Ghrelin, like its synthetic counterparts, the growth hormone (GH) secretagogues, has been shown to markedly stimulate adrenocorticotrophic hormone (ACTH) and cortisol secretion in humans and the ACTH-releasing effect of GH secretagogues is even greater in patients with pituitary ACTH-secreting tumours.
  • The aim of the present study was to evaluate the effect of ghrelin on ACTH secretion by human pituitary corticotroph tumours in vitro to test the functionality of this circuit.
  • Nine ACTH-secreting pituitary tumours (four microadenomas, five macroadenomas) were collected during surgery and incubated with 10-100 nM human ghrelin or with 10 nM human corticotrophin-releasing hormone (CRH).
  • Control experiments were performed in rat anterior pituitary primary cultures.
  • ACTH secretion was assessed after 4 h and 24 h incubation by immunometric assay.
  • After 4 h of incubation with ghrelin, medium ACTH concentrations were two- to ten-fold higher compared to ACTH concentrations in unstimulated wells.
  • The ACTH-releasing effect of ghrelin was significantly less than the response elicited by 10 nM CRH (up to 40-fold) Similar results were obtained after 24 h of incubation and a superimposable response pattern was observed in rat anterior pituitary primary cultures.
  • The present study demonstrates that the endogenous GH secretagogue, ghrelin, stimulates ACTH secretion directly from human tumoural corticotrophs, as well as from normal rat pituitary, and indicates that the marked ACTH release elicited by ghrelin in patients with Cushing's disease in vivo is due, at least in part, to its action on the pituitary tumour.
  • Moreover, these data uphold the concept of a functional intratumoural ghrelin paracrine circuit in human corticotroph adenomas.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / secretion. Adenoma / secretion. Adrenocorticotropic Hormone / secretion. Corticotrophs / secretion. Peptide Hormones / physiology
  • [MeSH-minor] Adult. Animals. Corticotropin-Releasing Hormone / physiology. Female. Ghrelin. Humans. In Vitro Techniques. Male. Middle Aged. Pituitary ACTH Hypersecretion / metabolism. Pituitary Gland, Anterior / metabolism. Rats

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  • (PMID = 17280594.001).
  • [ISSN] 0953-8194
  • [Journal-full-title] Journal of neuroendocrinology
  • [ISO-abbreviation] J. Neuroendocrinol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Ghrelin; 0 / Peptide Hormones; 9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone
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100. Gnjidić Z, Sajko T, Kudelić N, Malenica M, Vizner B, Vrkljan M, Hat J, Rumboldt Z: Reversible "brain atrophy" in patients with Cushing's disease. Coll Antropol; 2008 Dec;32(4):1165-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reversible "brain atrophy" in patients with Cushing's disease.
  • During the past 25 years, we came across 60 patients with corticotroph pituitary adenomas and Cushing's disease.
  • Neuroradiological examination showed prominent volume loss of the brain parenchyma, unexpected for the patient's age.
  • This "brain atrophy" appeared to regress after surgical removal of pituitary adenoma and normalization of cortisol level.
  • Observed difference between degree of "brain atrophy" in the Cushing's disease group and in the control group was statistically significant (p < 0.001).
  • The degree of "brain atrophy" correlated well with the duration of Cushing's disease.
  • Partial reversibility of "brain atrophy" was noticed during the 2nd, 3rd and 4th year after surgery and normalization of cortisol level.
  • Increased cortisol level is one of the causative factors in pathogenesis of "brain atrophy".
  • Loss of brain volume is at least partially reversible after normalization of cortisol levels.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / pathology. Adenoma / pathology. Brain / pathology. Pituitary ACTH Hypersecretion / pathology

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  • (PMID = 19149224.001).
  • [ISSN] 0350-6134
  • [Journal-full-title] Collegium antropologicum
  • [ISO-abbreviation] Coll Antropol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Croatia
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